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Journal articles on the topic 'Myocardial remodeling'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 May 2022

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1

Hellawell, Jennifer L., and Kenneth B. Margulies. "Myocardial Reverse Remodeling." Cardiovascular Therapeutics 30, no. 3 (November 25, 2010): 172–81. http://dx.doi.org/10.1111/j.1755-5922.2010.00247.x.

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2

Ushakov, Alexey, Vera Ivanchenko, and Alina Gagarina. "Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling." Current Cardiology Reviews 16, no. 1 (January 28, 2020): 11–24. http://dx.doi.org/10.2174/1573403x15666190509090832.

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The article represents literature review dedicated to molecular and cellular mechanisms underlying clinical manifestations and outcomes of acute myocardial infarction. Extracellular matrix adaptive changes are described in detail as one of the most important factors contributing to healing of damaged myocardium and post-infarction cardiac remodeling. Extracellular matrix is reviewed as dynamic constantly remodeling structure that plays a pivotal role in myocardial repair. The role of matrix metalloproteinases and their tissue inhibitors in fragmentation and degradation of extracellular matrix as well as in myocardium healing is discussed. This review provides current information about fibroblasts activity, the role of growth factors, particularly transforming growth factor β and cardiotrophin-1, colony-stimulating factors, adipokines and gastrointestinal hormones, various matricellular proteins. In conclusion considering the fact that dynamic transformation of extracellular matrix after myocardial ischemic damage plays a pivotal role in myocardial infarction outcomes and prognosis, we suggest a high importance of further investigation of mechanisms underlying extracellular matrix remodeling and cell-matrix interactions in cardiovascular diseases.
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3

Bhattacharya, Aniket, Nadia Al-Sammarraie, Mengistu G. Gebere, John Johnson, John F. Eberth, and Mohamad Azhar. "Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development." Journal of Cardiovascular Development and Disease 8, no. 3 (March 2, 2021): 26. http://dx.doi.org/10.3390/jcdd8030026.

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Among the three transforming growth factor beta (TGFβ) ligands, TGFβ2 is essential for heart development and is produced by multiple cell types, including myocardium. Heterozygous mutations in TGFB2 in patients of connective tissue disorders result in congenital heart defects and adult valve malformations, including mitral valve prolapse (MVP) with or without regurgitation. Tgfb2 germline knockout fetuses exhibit multiple cardiac defects but the role of myocardial-TGFβ2 in heart development is yet to be elucidated. Here, myocardial Tgfb2 conditional knockout (CKO) embryos were generated by crossing Tgfb2flox mice with Tgfb2+/−; cTntCre mice. Tgfb2flox/− embryos were normal, viable. Cell fate mapping was done using dual-fluorescent mT/mG+/− mice. Cre-mediated Tgfb2 deletion was assessed by genomic PCR. RNAscope in situ hybridization was used to detect the loss of myocardial Tgfb2 expression. Histological, morphometric, immunohistochemical, and in situ hybridization analyses of CKOs and littermate controls at different stages of heart development (E12.5–E18.5) were used to determine the role of myocardium-derived TGFβ2 in atrioventricular (AV) cushion remodeling and myocardial development. CKOs exhibit a thin ventricular myocardium, AV cushion remodeling defects and developed incomplete AV septation defects. The loss of myocardial Tgfb2 resulted in impaired cushion maturation and dysregulated cell death. Phosphorylated SMAD2, a surrogate for TGFβ signaling, was “paradoxically” increased in both AV cushion mesenchyme and ventricular myocardium in the CKOs. Our results indicate that TGFβ2 produced by cardiomyocytes acting as cells autonomously on myocardium and via paracrine signaling on AV cushions are required for heart development.
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4

Honjo, Haruo. "Myocardial Remodeling and Arrhythmogenesis." Japanese Journal of Electrocardiology 34, no. 1 (2014): 37–44. http://dx.doi.org/10.5105/jse.34.37.

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5

Gropler, R. J., R. S. B. Beanlands, V. Dilsizian, E. D. Lewandowski, F. S. Villanueva, and M. C. Ziadi. "Imaging Myocardial Metabolic Remodeling." Journal of Nuclear Medicine 51, Supplement_1 (May 1, 2010): 88S—101S. http://dx.doi.org/10.2967/jnumed.109.068197.

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6

RAO, VIJAY U., and FRANCIS G. SPINALE. "Controlling Myocardial Matrix Remodeling." Cardiology in Review 7, no. 3 (May 1999): 136–43. http://dx.doi.org/10.1097/00045415-199905000-00010.

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7

Nadruz, W. "Myocardial remodeling in hypertension." Journal of Human Hypertension 29, no. 1 (May 8, 2014): 1–6. http://dx.doi.org/10.1038/jhh.2014.36.

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8

Vasques-Nóvoa, Francisco, António Angélico-Gonçalves, Nuno Bettencourt, Adelino F. Leite-Moreira, and Roberto Roncon-Albuquerque. "Myocardial Edema and Remodeling." Journal of the American College of Cardiology 75, no. 12 (March 2020): 1497–98. http://dx.doi.org/10.1016/j.jacc.2019.12.071.

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9

Cokkinos, Dennis V., and Costas Pantos. "Myocardial remodeling, an overview." Heart Failure Reviews 16, no. 1 (September 26, 2010): 1–4. http://dx.doi.org/10.1007/s10741-010-9192-4.

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10

Chaanine, Antoine H. "Autophagy and Myocardial Remodeling." Journal of the American College of Cardiology 71, no. 18 (May 2018): 2011–14. http://dx.doi.org/10.1016/j.jacc.2018.02.067.

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11

González, Arantxa, Susana Ravassa, Begoña López, María U. Moreno, Javier Beaumont, Gorka San José, Ramón Querejeta, Antoni Bayés-Genís, and Javier Díez. "Myocardial Remodeling in Hypertension." Hypertension 72, no. 3 (September 2018): 549–58. http://dx.doi.org/10.1161/hypertensionaha.118.11125.

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12

Tomimatsu, Masashi, Kosei Yokota, Shunsuke Kominami, Shota Tanaka, Makiko Maeda, Yoshiaki Okada, Masanori Obana, and Yasushi Fujio. "TGFβ3 exacerbates myocardial remodeling after myocardial infarction." Proceedings for Annual Meeting of The Japanese Pharmacological Society 95 (2022): 1—O—036. http://dx.doi.org/10.1254/jpssuppl.95.0_1-o-036.

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13

Mondaca-Ruff, David, Patricio Araos, Cristián E. Yañez, Ulises F. Novoa, Italo G. Mora, María Paz Ocaranza, and Jorge E. Jalil. "Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension." Journal of Cardiovascular Pharmacology and Therapeutics 26, no. 6 (October 8, 2021): 724–35. http://dx.doi.org/10.1177/10742484211053109.

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Background: Thiazides are one of the most common antihypertensive drugs used for hypertension treatment and hydrochlorothiazide (HCTZ) is the most frequently used diuretic for hypertension treatment. The Rho/Rho-kinase (ROCK) path plays a key function in cardiovascular remodeling. We hypothesized that in preclinical hypertension HCTZ reduces myocardial ROCK activation and consequent myocardial remodeling. Methods: The preclinical model of deoxycorticosterone (DOCA)-salt hypertension was used (Sprague–Dawley male rats). After 3 weeks, in 3 different groups: HCTZ, the ROCK inhibitor fasudil or spironolactone was added (3 weeks). After 6 weeks myocardial hypertrophy and fibrosis, cardiac levels of profibrotic proteins, mRNA levels (RT PCR) of pro remodeling and pro oxidative molecules and ROCK activity were determined. Results: Blood pressure, myocardial hypertrophy and fibrosis were reduced significantly by HCTZ, fasudil and spironolactone. In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-β1 and gene expression of pro-remodeling molecules TGF-β1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone. ROCK activity in the myocardium was increased by 54% ( P < 0.05) as related to the sham group and HCTZ, spironolactone and fasudil, reduced ROCK activation to control levels. Conclusions: HCTZ reduced pathologic LVH by controlling blood pressure, hypertrophy and myocardial fibrosis and by decreasing myocardial ROCK activation, expression of pro remodeling, pro fibrotic and pro oxidative genes. In hypertension, the observed effects of HCTZ on the myocardium might explain preventive outcomes of thiazides in hypertension, specifically on LVH regression and incident heart failure.
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14

Chen, Kai, Yiqing Guan, Yunci Ma, Dongling Quan, Jingru Zhang, Shaoyu Wu, Xin Liu, Lin Lv, and Guohua Zhang. "Danshenol A Alleviates Hypertension-Induced Cardiac Remodeling by Ameliorating Mitochondrial Dysfunction and Suppressing Reactive Oxygen Species Production." Oxidative Medicine and Cellular Longevity 2019 (September 11, 2019): 1–18. http://dx.doi.org/10.1155/2019/2580409.

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Current therapeutic approaches have a limited effect on cardiac remodeling, which is characteristic of cardiac fibrosis and myocardial hypertrophy. In this study, we examined whether Danshenol A (DA), an active ingredient extracted from the traditional Chinese medicine Radix Salviae, can attenuate cardiac remodeling and clarified the underlying mechanisms. Using the spontaneously hypertensive rat (SHR) as a cardiac remodeling model, DA ameliorated blood pressure, cardiac injury, and myocardial collagen volume and improved cardiac function. Bioinformatics analysis revealed that DA might attenuate cardiac remodeling through modulating mitochondrial dysfunction and reactive oxygen species. DA repaired the structure/function of the mitochondria, alleviated oxidative stress in the myocardium, and restored apoptosis of cardiomyocytes induced by angiotensin II. Besides, DA inhibited mitochondrial redox signaling pathways in both the myocardium and cardiomyocytes. Thus, our study suggested that DA attenuates cardiac remodeling induced by hypertension through modulating mitochondrial dysfunction and reactive oxygen species.
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15

Morariu, Mirabela, Diana Opincariu, and Alexandra Stănescu. "Perfusion Computed Tomography for the Assessment of Myocardial Viability — a Case Series." Journal of Interdisciplinary Medicine 1, no. 1 (June 1, 2016): 83–87. http://dx.doi.org/10.1515/jim-2016-0016.

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Abstract Myocardial viability plays an important role in preventing the development of left ventricular remodeling following an acute myocardial infarction. A preserved viability in the infarcted area has been demonstrated to be associated with a lower amplitude of the remodeling process, while the extent of the non-viable myocardium is directly correlated with the amplitude of the remodeling process. A number of methods are currently in use for the quantification of the viable myocardium, and some of them are based on the estimation of myocardial perfusion during pharmacologic stress. 64-slice Multi-detector Computed Tomography (MDCT) during vasodilator stress test, associated with CT Coronary Angiography (CCTA) has a high diagnostic accuracy in evaluating myocardial perfusion. In this article, we present a sequence of 3 clinical cases that presented with symptoms of myocardial ischemia, who underwent 64-slice MDCT imaging at rest and during adenosine stress test, in order to assess the extent of the hypoperfused myocardial areas. Coronary artery anatomy and the Coronary Calcium Score was assessed for all 3 patients by performing CT Coronary Angiography. The combination of CT Angiography and adenosine stress CT myocardial perfusion imaging can accurately detect atherosclerosic lesions that cause perfusion abnormalities, compared with the combination of invasive angiography and single-photon emission computed tomography (SPECT).
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16

Bukatov, Vladislav V., and Olga A. Osipova. "Peculiarities of myocardial remodeling in patients of different age groups 6 months after myocardial infarction." Человек и его здоровье 24, no. 4 (2021): 34–43. http://dx.doi.org/10.21626/vestnik/2021-4/05.

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Objective. To assess the nature of changes in the types of myocardial remodeling of the left ventricle in patients of middle, elderly and senile age with acute ST-segment elevation myocardial infarction within 6 months after successful revascularization. Materials and methods. The study included 132 patients with a diagnosis of acute ST-segment elevation myocardial infarction, in combination with arterial hypertension who were divided into 3 groups depending on age: middle-aged pa-tients (45- 59) – 48 people, elderly patients (60-74) – 44 people, senile patients (75-89) – 40 people. The type of left ventricular remodeling was assessed by determining the relative wall thickness and mass index of the left ventricular myocardium with doppler echocardiography in the first 12 hours after the onset of anginal syndrome, and after 6 months. All patients underwent percutaneous coronary intervention. Results. It was found that initially with the development of acute myocardial infarction, senile patients more often had eccentric left ventricular hypertrophy (in 25%) than patients of middle (6%) and elderly age (11%). After 6 months, in middle-aged patients, the type of remodeling eccentric hypertrophy increased to 14%, in the elderly – up to 23%, in senile patients – up to 50%. Conclusion. In patients who have undergone acute myocardial infarction against the background of traditional therapy and rehabilitation, there are changes in the types of left ventricular myocardial remodeling: eccentric hypertrophy increases in middle age up to 14%, in the elderly – up to 23%, in senile age – up to 50%.
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17

Jain, Mohit, Ronglih Liao, Bruno K. Podesser, Soeun Ngoy, Carl S. Apstein, and Franz R. Eberli. "Influence of gender on the response to hemodynamic overload after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2544—H2550. http://dx.doi.org/10.1152/ajpheart.00338.2002.

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After myocardial infarction (MI), the left ventricle (LV) undergoes ventricular remodeling characterized by progressive global dilation, infarct expansion, and compensatory hypertrophy of the noninfarcted myocardium. Little attention has been given to the response of remodeling myocardium to additional hemodynamic overload. Studies have indicated that gender may influence remodeling and the response to both MI and hemodynamic overload. We therefore determined 1) structural and function consequences of superimposing hemodynamic overload (systemic hypertension) on remodeling myocardium after a MI and 2) the potential influence of gender on this remodeling response. Male and female Dahl salt-sensitive and salt-resistant rats underwent coronary ligation, resulting in similar degrees of MI. One week post-MI, all rats were placed on a high-salt diet. Four groups were then studied 4 wk after initiation of high-salt feeding: MI female, MI female + hypertension, MI male, and MI male + hypertension. Hypertension-induced pressure overload resulted in additional comparable degrees of myocardial hypertrophy in both females and males. In females, hypertension post-MI resulted in concentric hypertrophy with no additional cavity dilation and no measurable scar thinning. In contrast, in males, hypertension post-MI resulted in eccentric hypertrophy, further LV cavity dilation, and scar thinning. Physiologically, concentric hypertrophy in post-MI hypertensive females resulted in elevated contractile function, whereas eccentrically hypertrophied males had no such increase. Female gender influences favorably the remodeling and physiological response to hemodynamic overload after large MI.
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18

Maslovskyi, V. Yu. "PECULIARITIES OF HEART RHYTHM DISORDERS AND VENTRICULAR REPOLARIZATION STATUS IN PATIENTS WITH MYOCARDIAL INFARCTION WITHOUT ST SEGMENT ELEVATION DEPENDING ON THE INDICATORS OF STRUCTURAL REMODELING OF THE LEFT VENTRICLE." Здобутки клінічної і експериментальної медицини, no. 4 (March 25, 2022): 29–33. http://dx.doi.org/10.11603/1811-2471.2021.v.i4.12702.

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Resume. Despite advances in the treatment of acute myocardial infarction in most developed countries, this pathology remains the leading cause of morbidity and mortality. The search for opportunities to predict the development of complications, study of remodeling processes and their impact on the development of electrical instability of the myocardium is currently considered as a promising area of ​​non-invasive diagnosis of myocardial infarction. Aim. To establish the features of cardiac arrhythmias and the condition of ventricular repolarization in patients with NSTEMI depending on the indicators of structural remodeling of the left ventricle. Materials and methods. We conducted a comprehensive study of 200 patients with NSTEMI aged 38 to 80 years. All patients were examined according to the current protocol of diagnosis and treatment of patients with acute coronary syndrome without ST-segment elevation and daily Holter ECG monitoring was performed for 3-5 days after hospitalization. Results. An increase in the left ventricular myocardial mass index and a change in the geometric model are associated with an increase in the probability of developing myocardial electrical instability, in particular extrasystoles of any topic and paroxysmal tachycardia. At the same time, changes in structural remodeling indicators did not reveal correlations with ventricular repolarization disorders in the early NSTEMI period. Conclusions. Evaluation of the indicators of structural remodeling of the ventricular myocardium in the early period of NSTEMI allows to predict the risk of electrical instability of the myocardium and to carry out appropriate preventive measures.
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19

Xiao, Yi, Jiling Zhao, Julian P. Tuazon, Cesar V. Borlongan, and Guolong Yu. "MicroRNA-133a and Myocardial Infarction." Cell Transplantation 28, no. 7 (April 14, 2019): 831–38. http://dx.doi.org/10.1177/0963689719843806.

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Myocardial infarction (MI) is the leading cause of morbidity and mortality in the world. The infarcted heart displays typical cell death cascades characterized by a loss of cells and fibrotic scarring in the myocardium. Cardiac hypertrophy and fibrosis largely contribute to ventricular wall thickening and stiffening, altogether defining an adverse cardiac remodeling that ultimately leads to impaired cardiac function and subsequent heart failure. Finding a strategy to promote therapeutic, instead of detrimental, cardiac remodeling may pose as a potent MI treatment. Accumulating evidence shows that microRNAs (miRNAs) may play an essential role in cardiovascular diseases. In particular, microRNA-133a (miR-133a) is one of the most abundant miRNAs in the heart. Multiple studies have demonstrated that miR-133a participates in the early pathology of MI, as well as in subsequent cardiac remodeling. In this review, we summarize recent research progress highlighting the regulatory effects of miR-133a in ischemic myocardial diseases, such as inhibiting angiogenesis, apoptosis, fibrosis, hypertrophy, and inflammation, while promoting therapeutic cardiac remodeling. The goal is to elicit a critical discussion on the translational direction of miRNA-mediated treatments towards a safe and effective MI therapy.
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20

Pessoa, Fernanda Gallinaro, Keila Fonseca, Charles Mady, Orlando N. Ribeiro, Adriana M. Oliveira-Fonoff, Vera Salemi, Paulo Saldiva, Fabio Fernandes, and Felix Ramires. "AIR POLLUTION IN MYOCARDIAL REMODELING." Journal of the American College of Cardiology 69, no. 11 (March 2017): 720. http://dx.doi.org/10.1016/s0735-1097(17)34109-8.

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21

Weber, Karl T., Christian G. Brilla, and Joseph S. Janicki. "Myocardial Remodeling and Pathologic Hypertrophy." Hospital Practice 26, no. 4 (April 15, 1991): 73–80. http://dx.doi.org/10.1080/21548331.1991.11704159.

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22

Lovegrove, Carol. "Concentric remodeling and myocardial dysfunction." Nature Clinical Practice Cardiovascular Medicine 2, no. 12 (December 2005): 610–11. http://dx.doi.org/10.1038/ncpcardio0355.

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23

Riaz, Sadaf, Asad Zeidan, and Fatima Mraiche. "Myocardial proteases and cardiac remodeling." Journal of Cellular Physiology 232, no. 12 (May 16, 2017): 3244–50. http://dx.doi.org/10.1002/jcp.25884.

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24

SWYNGHEDAUW, BERNARD. "Molecular Mechanisms of Myocardial Remodeling." Physiological Reviews 79, no. 1 (January 1, 1999): 215–62. http://dx.doi.org/10.1152/physrev.1999.79.1.215.

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Swynghedauw, Bernard. Molecular Mechanisms of Myocardial Remodeling. Physiol. Rev. 79: 215–262, 1999. — “Remodeling” implies changes that result in rearrangement of normally existing structures. This review focuses only on permanent modifications in relation to clinical dysfunction in cardiac remodeling (CR) secondary to myocardial infarction (MI) and/or arterial hypertension and includes a special section on the senescent heart, since CR is mainly a disease of the elderly. From a biological point of view, CR is determined by 1 ) the general process of adaptation which allows both the myocyte and the collagen network to adapt to new working conditions; 2) ventricular fibrosis, i.e., increased collagen concentration, which is multifactorial and caused by senescence, ischemia, various hormones, and/or inflammatory processes; 3) cell death, a parameter linked to fibrosis, which is usually due to necrosis and apoptosis and occurs in nearly all models of CR. The process of adaptation is associated with various changes in genetic expression, including a general activation that causes hypertrophy, isogenic shifts which result in the appearance of a slow isomyosin, and a new Na+-K+-ATPase with a low affinity for sodium, reactivation of genes encoding for atrial natriuretic fator and the renin-angiotensin system, and a diminished concentration of sarcoplasmic reticulum Ca2+-ATPase, β-adrenergic receptors, and the potassium channel responsible for transient outward current. From a clinical point of view, fibrosis is for the moment a major marker for cardiac failure and a crucial determinant of myocardial heterogeneity, increasing diastolic stiffness, and the propensity for reentry arrhythmias. In addition, systolic dysfunction is facilitated by slowing of the calcium transient and the downregulation of the entire adrenergic system. Modifications of intracellular calcium movements are the main determinants of the triggered activity and automaticity that cause arrhythmias and alterations in relaxation.
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25

Margulies, Kenneth B. "Blocking Stretch-Induced Myocardial Remodeling." Circulation Research 93, no. 11 (November 28, 2003): 1020–22. http://dx.doi.org/10.1161/01.res.0000105922.61310.d4.

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26

Prastein, Deyanira J., Ahmet Kilic, Tomas Ayala, Zhongjun Wu, and Bartley P. Griffith. "MYOCARDIAL STRAIN MAP OF REMODELING." ASAIO Journal 51, no. 2 (March 2005): 29A. http://dx.doi.org/10.1097/00002480-200503000-00113.

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27

Ajijola, Olujimi A., and Kalyanam Shivkumar. "Neural Remodeling and Myocardial Infarction." Journal of the American College of Cardiology 59, no. 10 (March 2012): 962–64. http://dx.doi.org/10.1016/j.jacc.2011.11.031.

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28

WEBER, K. "Angiotensin II and myocardial remodeling." Journal of Molecular and Cellular Cardiology 21 (May 1989): S28. http://dx.doi.org/10.1016/0022-2828(89)90945-0.

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29

Sharpe, Norman. "Ventricular remodeling following myocardial infarction." American Journal of Cardiology 70, no. 10 (October 1992): 20–26. http://dx.doi.org/10.1016/0002-9149(92)91354-7.

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30

Torres, William M., Julia Jacobs, Heather Doviak, Shayne C. Barlow, Michael R. Zile, Tarek Shazly, and Francis G. Spinale. "Regional and temporal changes in left ventricular strain and stiffness in a porcine model of myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 4 (October 1, 2018): H958—H967. http://dx.doi.org/10.1152/ajpheart.00279.2018.

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The aim of the present study was to serially track how myocardial infarction (MI) impacts regional myocardial strain and mechanical properties of the left ventricle (LV) in a large animal model. Post-MI remodeling has distinct regional effects throughout the LV myocardium. Regional quantification of LV biomechanical behavior could help explain changes in global function and thus advance clinical assessment of post-MI remodeling. The present study is based on a porcine MI model to characterize LV biomechanics over 28 days post-MI via speckle-tracking echocardiography (STE). Regional myocardial strain and strain rate were recorded in the circumferential, radial, and longitudinal directions at baseline and at 3, 14, and 28 days post-MI. Regional myocardial wall stress was calculated using standard echocardiographic metrics of geometry and Doppler-derived hemodynamic measurements. Regional diastolic myocardial stiffness was calculated from the resultant stress-strain relations. Peak strain and phasic strain rates were nonuniformly reduced throughout the myocardium post-MI, whereas time to peak strain was increased to a similar degree in the MI region and border zone by 28 days post-MI. Elevations in diastolic myocardial stiffness in the MI region plateaued at 14 days post-MI, after which a significant reduction in MI regional stiffness in the longitudinal direction occurred between 14 and 28 days post-MI. Post-MI biomechanical changes in the LV myocardium were initially limited to the MI region but nonuniformly extended into the neighboring border zone and remote myocardium over 28 days post-MI. STE enabled quantification of regional and temporal differences in myocardial strain and diastolic stiffness, underscoring the potential of this technique for clinical assessment of post-MI remodeling. NEW & NOTEWORTHY For the first time, speckle-tracking echocardiography was used to serially track regional biomechanical behavior and mechanical properties postmyocardial infarction (post-MI). We found that changes initially confined to the MI region extended throughout the myocardium in a nonuniform fashion over 28 days post-MI. Speckle-tracking echocardiography-based evaluation of regional changes in left ventricular biomechanics could advance both clinical assessment of left ventricular remodeling and therapeutic strategies that target aberrant biomechanical behavior post-MI.
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Wang, Hui, Yuqin Zhang, Shuwen Guo, Jiani Wu, Wang’ou Lin, Binyue Zhang, Pengfei Feng, et al. "Effects of Yiqi Huoxue Decoction on Post-Myocardial Infarction Cardiac Nerve Remodeling and Cardiomyocyte Hypertrophy in Rats." Evidence-Based Complementary and Alternative Medicine 2021 (August 21, 2021): 1–16. http://dx.doi.org/10.1155/2021/5168574.

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Myocardial infarction can lead to ventricular remodeling and arrhythmia, which is closely related to nerve remodeling. Our previous study found that Yiqi Huoxue decoction (YQHX) can improve ventricular remodeling and reduce myocardial damage. Therefore, in this study, we observed the effect of YQHX on cardiac neural remodeling and cardiomyocyte hypertrophy and its possible mechanism. This research is composed of two parts: animal and H9c2 cells experiments. The animal model of acute myocardial infarction was established by ligating the left anterior descending coronary artery in Sprague Dawley (SD) rats. H9c2 cells were placed in 94% N2, 5% CO2, and 1% O2 hypoxic environment for 12 hours to replicate the hypoglycemic hypoxia model. The experimental results showed that, compared with the MI group, YQHX can significantly improve heart function after myocardial infarction and reduce nerve remodeling and myocardial hypertrophy. Pathological structure observation demonstrated reducing myocardial tissue damage and decreasing of cell cross-sectional area, diameter, and circumference. The positive rate of TH declined apparently, and the sympathetic nerve density was lower than that of the MI group. After YQHX was given for 28 days, the proneural remodeling factors TH, NGF, and GAP43 in the marginal zone of infarction and stellate ganglion decreased obviously while the inhibitory nerve remodeling factor Sema-3A increased. The myocardial hypertrophic protein ANP and β-MHC were also significantly inhibited with p-ERK1/2 protein expression level prominently reduced. There was no difference between the YQHX group and the Meto group. After myocardial infarction, nerve remodeling was seen in the marginal area of infarction and stellate ganglion, and the neuropeptides released by which promoted myocardial hypertrophy. The mechanism may be related to the ERK1/2 signaling pathway. YQHX could regulate the ERK1/2 signaling pathway, inhibit the release of nerve remodeling factors and myocardial hypertrophy protein to reduce nerve remodeling, and relieve myocardial hypertrophy.
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32

Ariyasinghe, Nethika R., Davi M. Lyra-Leite, and Megan L. McCain. "Engineering cardiac microphysiological systems to model pathological extracellular matrix remodeling." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 4 (October 1, 2018): H771—H789. http://dx.doi.org/10.1152/ajpheart.00110.2018.

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Many cardiovascular diseases are associated with pathological remodeling of the extracellular matrix (ECM) in the myocardium. ECM remodeling is a complex, multifactorial process that often contributes to declines in myocardial function and progression toward heart failure. However, the direct effects of the many forms of ECM remodeling on myocardial cell and tissue function remain elusive, in part because conventional model systems used to investigate these relationships lack robust experimental control over the ECM. To address these shortcomings, microphysiological systems are now being developed and implemented to establish direct relationships between distinct features in the ECM and myocardial function with unprecedented control and resolution in vitro. In this review, we will first highlight the most prominent characteristics of ECM remodeling in cardiovascular disease and describe how these features can be mimicked with synthetic and natural biomaterials that offer independent control over multiple ECM-related parameters, such as rigidity and composition. We will then detail innovative microfabrication techniques that enable precise regulation of cellular architecture in two and three dimensions. We will also describe new approaches for quantifying multiple aspects of myocardial function in vitro, such as contractility, action potential propagation, and metabolism. Together, these collective technologies implemented as cardiac microphysiological systems will continue to uncover important relationships between pathological ECM remodeling and myocardial cell and tissue function, leading to new fundamental insights into cardiovascular disease, improved human disease models, and novel therapeutic approaches.
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Zheng, Wei, Robert M. Weiss, Xinguo Wang, Ruifeng Zhou, Angie M. Arlen, Li Lei, Eric Lazartigues, and Robert J. Tomanek. "DITPA stimulates arteriolar growth and modifies myocardial postinfarction remodeling." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1994—H2000. http://dx.doi.org/10.1152/ajpheart.00991.2003.

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Myocardial infarction (MI) is characterized by ventricular remodeling, hypertrophy of the surviving myocardium, and an insufficient angiogenic response. Thyroxine is a powerful stimulus for myocardial angiogenesis. Male rats that underwent coronary artery ligation and subsequent MI were given 3,5-diiodothyropropionic acid (DITPA; MI+DITPA group) during a 3-wk period. We evaluated ventricular remodeling using echocardiography and histology and myocardial vessel growth using image analysis. Protein expression was assessed using Western blotting and immunohistochemistry. This study tested the hypothesis that the thyroxine analog DITPA facilitates angiogenesis and influences postinfarction remodeling in the surviving hypertrophic myocardium. The increase in the region of akinesis (infarct expansion) was blunted in the MI+DITPA rats compared with the MI group (3 vs. 21%); the treated rats had smaller percent increases in the left ventricular (LV) volume (64 ± 14 vs. 95 ± 12) and the LV volume-to-mass ratio (47 ± 13 vs. 84 ± 10) as well as a blunted decrease in ejection fraction (–9 ± 8 vs. –30 ± 7%). Arteriolar length density was higher after treatment in the largest (>50% of the free wall) infarcts (64 ± 3 vs. 43 ± 7). Angiogenic growth factors [vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF)] and the angiopoietin receptor tyrosine kinase with immunoglobulin and epidermal growth factor homology domains (Tie-2) values were elevated during the first week after infarction. DITPA did not cause additional increases in VEGF or Tie-2 values but did induce an increase in bFGF value after 3 days of treatment. This study provides the first evidence for an anatomical basis, i.e., attenuated ventricular remodeling and arteriolar growth, for improved function attributed to DITPA therapy of the infarcted heart. The favorable influences of DITPA on LV remodeling after large infarction are principally due to border zone preservation.
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Kytikova, O. Yu, T. P. Novgorodtseva, М. V. Antonyuk, Yu K. Denisenko, and O. V. Atamas. "Nerve growth factor and post-infarction cardiac remodeling." Acta Biomedica Scientifica 7, no. 2 (May 23, 2022): 113–24. http://dx.doi.org/10.29413/abs.2022-7.2.13.

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The prevalence of sudden death from chronic heart failure and cardiac arrhythmias caused by myocardial infarction is a complex problem in cardiology. Post-infarction cardiac remodeling occurs after myocardial infarction. This compensatory-adaptive reaction, regulated by mechanical, neurohumoral and genetic factors, includes the structural and functional changes of cardiomyocytes, stromal elements and extracellular matrix, geometry and architectonics of the left ventricular cavity. Adverse left ventricular remodeling is associated with heart failure and increased mortality. The concept of post-infarction cardiac remodeling is an urgent problem, since the mechanisms of development and progression of adverse post-infarction changes in the myocardium are completely unexplored. In recent years, the scientist attention has been focused on neurotrophic factors involved in the sympathetic nervous system and the vascular system remodeling after myocardial infarction. Nerve growth factor (NGF) is a protein from the neurotrophin family that is essential for the survival and development of sympathetic and sensory neurons, which also plays an important role in vasculogenesis. Acute myocardial infarction and heart failure are characterized by changes in the expression and activity of neurotrophic factors and their receptors, affecting the innervation of the heart muscle, as well as having a direct effect on cardiomyocytes, endothelial and smooth muscle vascular cells. The identification of the molecular mechanisms involved in the interactions between cardiomyocytes and neurons, as well as the study of the effects of NGF in the cardiovascular system, will improve understanding of the cardiac remodeling mechanism. This review summarizes the available scientific information (2019–2021) about mechanisms of the link between post-infarction cardiac remodeling and NGF functions.
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Liang, Yulei, Zhifang Zhang, Tianyuan Lv, Zhengxian Shen, Xin Wang, Shiling Lv, Dongyun Sun, and Chaoyi Fang. "Moxibustion at CV 8 alleviates the myocardial inflammatory response in rats with long-term exercise-induced fatigue through inhibition of the p38 MAPK/NF-κβ signaling pathway." Acupuncture & Electro-Therapeutics Research 45, no. 1 (August 24, 2020): 31–38. http://dx.doi.org/10.3727/036012920x15958782196817.

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Pathological cardiac remodeling is an important cause of sudden cardiac death and other cardiovascular diseases in athletes. Unfortunately, people involved in long-term intense endurance exercise (especially professional athletes) do not fully understand the cause and health risks of pathological cardiac remodeling, resulting in pathological cardiac remodeling developing into irreversible damage, which seriously affects sports careers and the postretirement life of athletes. Studies have shown that myocardial inflammation caused by long-term and repeated high-intensity exercise is a prerequisite for inducing pathological remodeling and that effective inhibition of inflammation can block or reverse the pathological process of pathological remodeling. This preliminary study showed that moxibustion at CV 8 inhibited the p38 mitogen-activated protein kinases/nuclear factor-κβ (p38 MAPK/NF-κβ) signaling pathway in myocardium, reduced the expression of cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor(TNF-α), significantly improved myocardial morphology and function in rats under going long-term and repeated high-intensity exercise, and effectively prevented pathological cardiac remodeling. Moxibustion at CV 8 provides a new physical therapy and experimental basis for the treatment of pathological cardiac remodeling in clinical practice.
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36

Oleynikov, V. E., Yu A. Barmenkova, E. V. Dushina, and A. V. Golubeva. "Relationship between electrical myocardial instability and postinfarction remodeling in patients with ST-segment elevation myocardial infarction." Kardiologiia 61, no. 10 (October 30, 2021): 14–25. http://dx.doi.org/10.18087/cardio.2021.10.n1626.

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Aim To study the clinical value of markers for myocardial electrical instability in combination with echocardiographic parameters for predicting the risk of cardiovascular complications (CVC) in the postinfarction period.Material and methods This study included 118 patients with ST segment elevation myocardial infarction (STEMI) and hemodynamically significant stenosis of one coronary artery. A percutaneous coronary intervention (PCI) with stenting of the infarct-related artery was performed for all patients. On day 7-9 and at 24 and 48 weeks after the treatment, ECG Holter monitoring was performed, which included analyses of ventricular late potentials, dispersion of QT interval duration, heart rate turbulence (HRT) and variability (HRV), and heart chronotropic load (HCL). At baseline and during postinfarction week 12, all patients underwent echocardiography with calculation of indexes of end-diastolic volume (iEDV) and end-systolic volume (iESV) to verify the signs of left ventricular (LV) myocardial remodeling. The criteria for LV pathological remodeling included increases in iEDV >20 % and/or iESV >15 % at 12 weeks after STEMI. The group without remodeling, R(-), consisted of 79 (67 %) patients and the group with signs of LV pathological remodeling, R(+), consisted of 39 (33 %) patients. Quality of life and achieved endpoints were evaluated during 144 weeks.Results By week 48 in group R(-), the stabilization of electrical processes in the myocardium was more pronounced as indicated by a decrease in HFLA by 12 % (р=0.004) and by a fourfold increase in RMS (р=0.047). Only in this group, the baroreflex sensitivity restored; pathological ТРС decreased from 20 to 5% (p=0.002) by the end of the active treatment. Stabilization of the repolarization phase duration in various parts of the myocardium was more active in patients without pathological remodeling as shown by decreases in disp QTa (р=0.009), disp QTe (р=0.03), sd QTa (р=0.006), and sd QTe (р=0.009). This was not observed in the group R(+). The recovery of vagosympathetic balance due to leveling the sympathetic component also was more effective in the group R(-), which was reflected in increased spectral and temporal HRV indexes (р<0.05). Both groups showed reduced HCL values at 24 weeks (р=0.047 and р=0.006); however, the HCL regression remained also at 48 weeks only in the group R(-) (р=0.006). Group R(-) patients reported higher quality of life (р=0.03) than group R(+) patients. Endpoints were achieved more frequently in the group R(+): 87.1 % vs. 27.8 % (odds ratio, 11.8; 95 % confidence interval, 4.6–30.8; р=0.00001).Conclusion Pathological myocardial remodeling in early postinfarction period is associated with electrophysiological instability of the myocardium, which results in the development of CVC and low quality of life in patients with STEMI.
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Gasparini, Stefania, Sonja Fonfara, Sarah Kitz, Udo Hetzel, and Anja Kipar. "Canine Dilated Cardiomyopathy: Diffuse Remodeling, Focal Lesions, and the Involvement of Macrophages and New Vessel Formation." Veterinary Pathology 57, no. 3 (March 3, 2020): 397–408. http://dx.doi.org/10.1177/0300985820906895.

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Dilated cardiomyopathy (DCM) is among the most common cardiac diseases in dogs. Its pathogenesis is not fully understood, but myocardial remodeling and inflammation are suspected to be involved. The present study aimed to characterize the pathological processes in canine DCM, investigating morphological changes in association with the expression of relevant cytokines and remodeling markers. The myocardium of 17 dogs with DCM and 6 dogs without cardiac diseases was histologically evaluated, and selected cases were further examined by immunohistochemistry, morphometry, and reverse transcription quantitative PCR. In DCM, the myocardium exhibited subtle but statistically significant diffuse quantitative changes. These comprised increased interstitial collagen deposition and macrophage numbers, as well as an overall reduced proportion of contractile tissue. This was accompanied by a significant increase in myocardial transcription of intracellular adhesion molecule (ICAM) 1, inflammatory cytokines, and remodeling enzymes. Laser microdissection showed that cardiomyocytes transcribed most relevant markers including ICAM-1, tumor necrosis factor α, transforming growth factor β (TGF-β), matrix metalloproteinase 2 (MMP-2), tissue inhibitor of MMP (TIMP) 1 and TIMP-2. In addition, there were multifocal cell-rich lesions characterized by fibrosis, neovascularization, macrophage infiltration, and cardiomyocyte degeneration. In these, macrophages were often found to express ICAM-1, TGF-β, and vascular endothelial growth factor; the former two were also expressed by cardiomyocytes. These results characterize the diffuse myocardial remodeling processes that occur in DCM. The observed multifocal cell-rich lesions might result from reduced tissue perfusion. Macrophages and cardiomyocytes seem to actively contribute to the remodeling processes, which ultimately lead to cardiac dilation and dysfunction. The precise role of the involved cells and the factors initiating the remodeling process still needs to be identified.
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Niccoli, Giampaolo, Rocco A. Montone, Borja Ibanez, Holger Thiele, Filippo Crea, Gerd Heusch, Heerajnarain Bulluck, et al. "Optimized Treatment of ST-Elevation Myocardial Infarction." Circulation Research 125, no. 2 (July 5, 2019): 245–58. http://dx.doi.org/10.1161/circresaha.119.315344.

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Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction.
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Dixon, J. A., R. C. Gorman, R. E. Stroud, S. Bouges, H. Hirotsugu, J. H. Gorman, T. P. Martens, et al. "Mesenchymal Cell Transplantation and Myocardial Remodeling After Myocardial Infarction." Circulation 120, no. 11_suppl_1 (September 14, 2009): S220—S229. http://dx.doi.org/10.1161/circulationaha.108.842302.

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Thackeray, James T., Henri C. Hupe, Yong Wang, Jens P. Bankstahl, Georg Berding, Tobias L. Ross, Johann Bauersachs, Kai C. Wollert, and Frank M. Bengel. "Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction." Journal of the American College of Cardiology 71, no. 3 (January 2018): 263–75. http://dx.doi.org/10.1016/j.jacc.2017.11.024.

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41

Zhang, Tian, Na Tang, Dongmei Xi, Yongli Zhao, Yongmin Liu, Lamei Wang, Yan Tang, Xiaoni Zhang, Hua Zhong, and Fang He. "Calcimimetic R568 improved cardiac remodeling by classic and novel renin-angiotensin system in spontaneously hypertensive rats." Experimental Biology and Medicine 244, no. 10 (June 3, 2019): 789–801. http://dx.doi.org/10.1177/1535370219854325.

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One major cause of cardiac mortality is heart disease caused by hypertension. The formation of cyclic adenosine monophosphate (cAMP) is inhibited by calcium-sensitive receptor (CaSR) activation which increases intracellular Ca2+ concentrations and suppresses renin release. As we know, renin-angiotensin system (RAS) is closely related to development of essential hypertension (EH). Therefore, we focused on exploring the roles of NPSR568 (R568)-activated CaSR in cardiac remodeling of spontaneously hypertensive rats (SHRs), as well as the activity of classic and novel RAS. Wistar-Kyoto rats (WKYs) and SHRs were treated by R568 for four and eight weeks, respectively, and their blood pressure (BP), echocardiographic values, heart-to-body weight ratio (HW/BW%), and left ventricle-to-body weight ratio (LVW/BW%) were evaluated. Then Masson’s trichrome staining and hematoxylin and eosin staining as well as RT-qPCR analysis of β-isoform of myosin heavy chain and brain natriuretic peptide mRNA expression were performed. A Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and analysis of apoptosis marker proteins were used to assess the extent of myocardial apoptosis. The CaSR expression and the activity of classic and novel RAS were examined by immunohistochemistry, western blotting, and enzyme-linked immunosorbent assay. The present study revealed that the development of hypertension was accompanied by increased BP, apoptosis, hypertrophy, and fibrosis, along with decreased expression of CaSR, decreased novel RAS, and increased classic RAS in myocardial tissues. R568 administration for four and eight weeks reduced BP and myocardial remodeling and reversed the low expression of CaSR; moreover, classic RAS was suppressed and novel RAS was activated in the myocardium. Taken together, these data indicate that R568 may effectively inhibit EH myocardial remodeling by inhibiting classic RAS and activating novel RAS in SHRs. Impact statement Our study reveals that low calcium-sensitive receptor (CaSR) expression is associated with the occurrence and development of essential hypertension-mediated myocardial remodeling. The activation of CaSR can reverse adverse myocardia remodeling by inhibiting local classical renin-angiotensin system (RAS) and activating novel RAS in cardiac tissues. CaSR is closely related to many cardiovascular diseases, but its specific mechanism remains not to be elucidated. To date, CaSR has not been investigated with regard to cardiovascular treatment; however, given the important relationship between CaSR and cardiovascular disease, CaSR regulators can be potential drugs for the treatment of cardiovascular disease.
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Schirone, Leonardo, Maurizio Forte, Silvia Palmerio, Derek Yee, Cristina Nocella, Francesco Angelini, Francesca Pagano, et al. "A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/3920195.

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Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.
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Saxena, Amit, Marcin Dobaczewski, Vikrant Rai, Zaffar Haque, Wei Chen, Na Li, and Nikolaos G. Frangogiannis. "Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 8 (October 15, 2014): H1233—H1242. http://dx.doi.org/10.1152/ajpheart.00328.2014.

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Regulatory T cells (Tregs) play a pivotal role in suppressing immune responses regulating behavior and gene expression in effector T cells, macrophages, and dendritic cells. Tregs infiltrate the infarcted myocardium; however, their role the inflammatory and reparative response after myocardial infarction remains poorly understood. We used FoxP3EGFP reporter mice to study Treg trafficking in the infarcted heart and examined the effects of Treg depletion on postinfarction remodeling using an anti-CD25 antibody. Moreover, we investigated the in vitro effects of Tregs on cardiac fibroblast phenotype and function. Low numbers of Tregs infiltrated the infarcted myocardium after 24–72 h of reperfusion. Treg depletion had no significant effects on cardiac dysfunction and scar size after reperfused myocardial infarction but accelerated ventricular dilation and accentuated apical remodeling. Enhanced myocardial dilation in Treg-depleted animals was associated with increased expression of chemokine (C-C motif) ligand 2 and accentuated macrophage infiltration. In vitro, Tregs modulated the cardiac fibroblast phenotype, reducing expression of α-smooth muscle actin, decreasing expression of matrix metalloproteinase-3, and attenuating contraction of fibroblast-populated collagen pads. Our findings suggest that endogenous Tregs have modest effects on the inflammatory and reparative response after myocardial infarction. However, the anti-inflammatory and matrix-preserving properties of Tregs may suggest a role for Treg-based cell therapy in the attenuation of adverse postinfarction remodeling.
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44

Pecherina, T. B., and A. G. Kutikhin. "Biomarkers of myocardial fibrosis and their genetic regulation in patients with heart failure." Russian Journal of Cardiology 25, no. 10 (November 18, 2020): 3933. http://dx.doi.org/10.15829/1560-4071-2020-3933.

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Currently, the development of chronic heart failure (CHF) is considered from the perspective of pathological structural remodeling of myocardium and fibrosis. Despite the widespread use of molecular genetic markers in clinical practice, only a small number of them are used to evaluate remodeling processes, as well as to predict potential complications associated with heart failure (HF). In addition, the relationship between many biomarkers with instrumental and histological confirmation of myocardial fibrosis has not yet been determined. Myocardial fibrosis remains quite debatable and controversial subject, which actualizes the further study of this direction. The discovery of pathogenetic and diagnostic markers of myocardial fibrosis could contribute to the development of targeted therapy. Of particular interest is the search for possible pathogenetic markers, since this is relevant for clinical practice.
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45

Liu, Chunping, Zhijin Fan, Dongyue He, Huiqi Chen, Shihui Zhang, Sien Guo, Bojun Zheng, et al. "Designer Functional Nanomedicine for Myocardial Repair by Regulating the Inflammatory Microenvironment." Pharmaceutics 14, no. 4 (March 31, 2022): 758. http://dx.doi.org/10.3390/pharmaceutics14040758.

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Acute myocardial infarction is a major global health problem, and the repair of damaged myocardium is still a major challenge. Myocardial injury triggers an inflammatory response: immune cells infiltrate into the myocardium while activating myofibroblasts and vascular endothelial cells, promoting tissue repair and scar formation. Fragments released by cardiomyocytes become endogenous “danger signals”, which are recognized by cardiac pattern recognition receptors, activate resident cardiac immune cells, release thrombin factors and inflammatory mediators, and trigger severe inflammatory responses. Inflammatory signaling plays an important role in the dilation and fibrosis remodeling of the infarcted heart, and is a key event driving the pathogenesis of post-infarct heart failure. At present, there is no effective way to reverse the inflammatory microenvironment in injured myocardium, so it is urgent to find new therapeutic and diagnostic strategies. Nanomedicine, the application of nanoparticles for the prevention, treatment, and imaging of disease, has produced a number of promising applications. This review discusses the treatment and challenges of myocardial injury and describes the advantages of functional nanoparticles in regulating the myocardial inflammatory microenvironment and overcoming side effects. In addition, the role of inflammatory signals in regulating the repair and remodeling of infarcted hearts is discussed, and specific therapeutic targets are identified to provide new therapeutic ideas for the treatment of myocardial injury.
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46

Gourine, Andrey V., Qingsong Hu, Paul R. Sander, Aleksandr I. Kuzmin, Nadia Hanafy, Svetlana A. Davydova, Dmitry V. Zaretsky, and Jianyi Zhang. "Interstitial purine metabolites in hearts with LV remodeling." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 2 (February 2004): H677—H684. http://dx.doi.org/10.1152/ajpheart.00305.2003.

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The myocardial ATP concentration is significantly decreased in failing hearts, which may be related to the progressive loss of the myocardial total adenine nucleotide pool. The total myocardial interstitial purine metabolites (IPM) in the dialysate of interstitial fluid could reflect the tissue ATP depletion. In rats, postmyocardial infarction (MI) left ventricular (LV) remodeling was induced by ligation of the coronary artery. Cardiac microdialysis was employed to assess changes of IPM in response to graded β-adrenergic stimulation with isoproterenol (Iso) in myocardium of hearts with post-MI LV remodeling (MI group) or hearts with sham operation (sham group). The dialysate samples were analyzed for adenosine, inosine, hypoxanthine, xanthine, and uric acid. LV volume was greater in the MI group (2.2 ± 0.2 ml/kg) compared with the sham group (1.3 ± 0.2 ml/kg, P < 0.05). Infarct size was 28 ± 4%. The baseline dialysate level of uric acid was higher in the MI group (18.9 ± 3.4 μmol) compared with the sham group (4.6 ± 0.7 μmol, P < 0.01). During and after Iso infusion, the dialysate levels of adenosine, xanthine, and uric acid were all significantly higher in the MI group. Thus the level of IPM is increased in hearts with postinfarction LV remodeling both at baseline and during Iso infusion. These results suggest that the decreased myocardial ATP level in hearts with post-MI LV remodeling may be caused by the chronic depletion of the total adenine nucleotide pool.
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47

Celic, Vera, Milica Dekleva, Anka Majstorovic, Nenad Radivojevic, Nada Kostic, and Zorica Caparevic. "Myocardial performance index: prediction and monitoring of remodeling and functioning of the left ventricle after first myocardial infarction." Medical review 63, no. 9-10 (2010): 652–55. http://dx.doi.org/10.2298/mpns1010652c.

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Introduction. Dynamic changing of left ventricular geometry and contractile state after acute myocardial infarction is responsible for various aspects of left ventricular remodeling and dysfunction. A number of studies have shown that myocardial performance index allows prediction of acute myocardial infarction complications. The objective of our study was to determine the power of myocardial performance index to predict and assess the severity of left ventricular remodeling, systolic and diastolic dysfunction after acute myocardial infarction over the long term. Material and methods. Echocardiography was performed within the first week of hospitalization, after one, three and six months in 77 patients with first acute myocardial infarction. At the end of the study the patients were divided into group A and B with mild and severe left ventricular remodeling, respectively. Results. Myocardial performance index was significantly lower in group A compared to B, at the beginning (0.62 vs. 0.75; p=0.002), and at the end of study (0, 60 vs. 0, 69; p=0.004). After six months, 31% of study patients developed LV systolic dysfunction with prevalence in group B (56% vs. 19%, p=0.002). Myocardial performance index ? 0.70 at first week after acute myocardial infarction is a strong predictive parameter for extensive early and late left ventricular remodeling and systolic dysfunction (p<0.05), but it is not a valuable predictor of diastolic failure. Discussion and conclusions. MPI obtained at first week of acute myocardial infarction was predictive for early and long term left ventricular remodeling and systolic dysfunction. Myocardial performance index had doubtful clinical use in assessing dynamics of remodeling and it was without clinical value in predicting diastolic function deterioration.
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Zakirova, A. N., R. G. Oganov, N. E. Zakirova, G. R. Klochkova, and F. S. Musina. "MYOCARDIAL REMODELING IN ISCHEMIC HEART DISEASE." Rational Pharmacotherapy in Cardiology 5, no. 1 (January 1, 2009): 42–45. http://dx.doi.org/10.20996/1819-6446-2009-5-1-42-45.

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49

Shim, Wan Joo, Chang Gyu Park, Young Hoon Kim, Hong Seog Seo, Dong Joo Oh, Jung Euy Park, and Young Moo Ro. "Ventricular Remodeling after Acute Myocardial Infarction." Korean Circulation Journal 23, no. 6 (1993): 921. http://dx.doi.org/10.4070/kcj.1993.23.6.921.

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50

M. Finch, Jennifer, and Jacob Joseph. "Homocysteine, Cardiovascular Inflammation, and Myocardial Remodeling." Cardiovascular & Hematological Disorders-Drug Targets 10, no. 4 (December 1, 2010): 241–45. http://dx.doi.org/10.2174/187152910793743887.

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