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Journal articles on the topic 'Heart – Hypertrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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1

Kang, Peter M., Patrick Yue, Zhilin Liu, Oleg Tarnavski, Natalya Bodyak, and Seigo Izumo. "Alterations in apoptosis regulatory factors during hypertrophy and heart failure." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (2004): H72—H80. http://dx.doi.org/10.1152/ajpheart.00556.2003.

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Cardiac hypertrophy from pathological stimuli often proceeds to heart failure, whereas cardiac hypertrophy from physiological stimuli does not. In this study, physiological hypertrophy was created by a daily exercise regimen and pathological hypertrophy was created from a high-salt diet in Dahl salt-sensitive rats. The rats continued on a high-salt diet progressed to heart failure associated with an increased rate of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. We analyzed primary cultures of these hearts and found that only cardiomyocytes made

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2

Liu, Yaoqiu, Yahui Shen, Jingai Zhu, et al. "Cardiac-Specific PID1 Overexpression Enhances Pressure Overload-Induced Cardiac Hypertrophy in Mice." Cellular Physiology and Biochemistry 35, no. 5 (2015): 1975–85. http://dx.doi.org/10.1159/000374005.

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Background/Aims: PID1 was originally described as an insulin sensitivity relevance protein, which is also highly expressed in heart tissue. However, its function in the heart is still to be elucidated. Thus this study aimed to investigate the role of PID1 in the heart in response to hypertrophic stimuli. Methods: Samples of human failing hearts from the left ventricles of dilated cardiomyopathy (DCM) patients undergoing heart transplants were collected. Transgenic mice with cardiomyocyte-specific overexpression of PID1 were generated, and cardiac hypertrophy was induced by transverse aortic co

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3

Kee, Hae Jin, and Hyun Kook. "Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/928326.

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Cardiac hypertrophy occurs in association with heart diseases and ultimately results in cardiac dysfunction and heart failure. Histone deacetylases (HDACs) are post-translational modifying enzymes that can deacetylate histones and non-histone proteins. Research with HDAC inhibitors has provided evidence that the class I HDACs are pro-hypertrophic. Among the class I HDACs, HDAC2 is activated by hypertrophic stresses in association with the induction of heat shock protein 70. Activated HDAC2 triggers hypertrophy by inhibiting the signal cascades of either Krüppel like factor 4 (KLF4) or inositol

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4

Hu, Chengyun, Feibiao Dai, Jiawu Wang, et al. "Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice." Oxidative Medicine and Cellular Longevity 2022 (January 29, 2022): 1–12. http://dx.doi.org/10.1155/2022/5067544.

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A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown acceler

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Sarkar, Sagartirtha, Douglas W. Leaman, Sudhiranjan Gupta, et al. "Cardiac Overexpression of Myotrophin Triggers Myocardial Hypertrophy and Heart Failure in Transgenic Mice." Journal of Biological Chemistry 279, no. 19 (2004): 20422–34. http://dx.doi.org/10.1074/jbc.m308488200.

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Cardiac hypertrophy and heart failure remain leading causes of death in the United States. Many studies have suggested that, under stress, myocardium releases factors triggering protein synthesis and stimulating myocyte growth. We identified and cloned myotrophin, a 12-kDa protein from hypertrophied human and rat hearts. Myotrophin (whose gene is localized on human chromosome 7q33) stimulates myocyte growth and participates in cellular interaction that initiates cardiac hypertrophyin vitro. In this report, we present data on the pathophysiological significance of myotrophinin vivo, showing the

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6

Qian, Yanxia, Mingming Zhang, Ningtian Zhou, et al. "A long noncoding RNA CHAIR protects the heart from pathological stress." Clinical Science 134, no. 13 (2020): 1843–57. http://dx.doi.org/10.1042/cs20200149.

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Abstract Mammalian genomes have been found to be extensively transcribed. In addition to classic protein coding genes, a large numbers of long noncoding genes (lncRNAs) have been identified, while their functions, especially in heart diseases, remain to be established. We hypothesized that heart failure progression is controlled by tissue-specific lncRNAs. In the present study, we found that the cardiac-enriched lncRNA 4632428C04Rik, named as cardiomyocyte hypertrophic associated inhibitory RNA (CHAIR), is dynamically regulated during heart development, is expressed at low levels in embryonic

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7

Zhang, Yan, Qiang Da, Siyi Cao, et al. "HINT1 (Histidine Triad Nucleotide-Binding Protein 1) Attenuates Cardiac Hypertrophy Via Suppressing HOXA5 (Homeobox A5) Expression." Circulation 144, no. 8 (2021): 638–54. http://dx.doi.org/10.1161/circulationaha.120.051094.

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Background: Cardiac hypertrophy is an important prepathology of, and will ultimately lead to, heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown. This study aims to elucidate the effects and mechanisms of HINT1 (histidine triad nucleotide–binding protein 1) in cardiac hypertrophy and heart failure. Methods: HINT1 was downregulated in human hypertrophic heart samples compared with nonhypertrophic samples by mass spectrometry analysis. Hint1 knockout mice were challenged with transverse aortic constriction surgery. Cardiac-specific overexpre

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8

SHANTZ, Lisa M., David J. FEITH та Anthony E. PEGG. "Targeted overexpression of ornithine decarboxylase enhances β-adrenergic agonist-induced cardiac hypertrophy". Biochemical Journal 358, № 1 (2001): 25–32. http://dx.doi.org/10.1042/bj3580025.

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These studies were designed to determine the consequences of constitutive overexpression of ornithine decarboxylase (ODC) in the heart. Induction of ODC is known to occur in response to agents that induce cardiac hypertrophy. However, it is not known whether high ODC levels are sufficient for the development of a hypertrophic phenotype. Transgenic mice were generated with cardiac-specific expression of a stable ODC protein using the α-myosin heavy-chain promoter. Founder lines with > 1000-fold overexpression of ODC in the heart were established, resulting in a 50-fold overaccumulation of pu

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9

Gu, Wei, Yutong Cheng, Su Wang, Tao Sun, and Zhizhong Li. "PHD Finger Protein 19 Promotes Cardiac Hypertrophy via Epigenetically Regulating SIRT2." Cardiovascular Toxicology 21, no. 6 (2021): 451–61. http://dx.doi.org/10.1007/s12012-021-09639-0.

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AbstractEpigenetic regulations essentially participate in the development of cardiomyocyte hypertrophy. PHD finger protein 19 (PHF19) is a polycomb protein that controls H3K36me3 and H3K27me3. However, the roles of PHF19 in cardiac hypertrophy remain unknown. Here in this work, we observed that PHF19 promoted cardiac hypertrophy via epigenetically targeting SIRT2. In angiotensin II (Ang II)-induced cardiomyocyte hypertrophy, adenovirus-mediated knockdown of Phf19 reduced the increase in cardiomyocyte size, repressed the expression of hypertrophic marker genes Anp and Bnp, as well as inhibited

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10

Funamoto, Masafumi, Yoichi Sunagawa, Yasufumi Katanasaka, et al. "Histone Acetylation Domains Are Differentially Induced during Development of Heart Failure in Dahl Salt-Sensitive Rats." International Journal of Molecular Sciences 22, no. 4 (2021): 1771. http://dx.doi.org/10.3390/ijms22041771.

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Histone acetylation by epigenetic regulators has been shown to activate the transcription of hypertrophic response genes, which subsequently leads to the development and progression of heart failure. However, nothing is known about the acetylation of the histone tail and globular domains in left ventricular hypertrophy or in heart failure. The acetylation of H3K9 on the promoter of the hypertrophic response gene was significantly increased in the left ventricular hypertrophy stage, whereas the acetylation of H3K122 did not increase in the left ventricular hypertrophy stage but did significantl

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11

Li, Wei-ming, Yi-fan Zhao, Guo-fu Zhu, et al. "Dual specific phosphatase 12 ameliorates cardiac hypertrophy in response to pressure overload." Clinical Science 131, no. 2 (2016): 141–54. http://dx.doi.org/10.1042/cs20160664.

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Pathological cardiac hypertrophy is an independent risk factor of heart failure. However, we still lack effective methods to reverse cardiac hypertrophy. DUSP12 is a member of the dual specific phosphatase (DUSP) family, which is characterized by its DUSP activity to dephosphorylate both tyrosine and serine/threonine residues on one substrate. Some DUSPs have been identified as being involved in the regulation of cardiac hypertrophy. However, the role of DUSP12 during pathological cardiac hypertrophy is still unclear. In the present study, we observed a significant decrease in DUSP12 expressio

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12

Bi, Hai-Lian, Xiao-Li Zhang, Yun-Long Zhang, et al. "The deubiquitinase UCHL1 regulates cardiac hypertrophy by stabilizing epidermal growth factor receptor." Science Advances 6, no. 16 (2020): eaax4826. http://dx.doi.org/10.1126/sciadv.aax4826.

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Pathological cardiac hypertrophy leads to heart failure (HF). The ubiquitin-proteasome system (UPS) plays a key role in maintaining protein homeostasis and cardiac function. However, research on the role of deubiquitinating enzymes (DUBs) in cardiac function is limited. Here, we observed that the deubiquitinase ubiquitin C-terminal hydrolase 1 (UCHL1) was significantly up-regulated in agonist-stimulated primary cardiomyocytes and in hypertrophic and failing hearts. Knockdown of UCHL1 in cardiomyocytes and mouse hearts significantly ameliorated cardiac hypertrophy induced by agonist or pressure

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13

Xie, Xin, Hai-Lian Bi, Song Lai та ін. "The immunoproteasome catalytic β5i subunit regulates cardiac hypertrophy by targeting the autophagy protein ATG5 for degradation". Science Advances 5, № 5 (2019): eaau0495. http://dx.doi.org/10.1126/sciadv.aau0495.

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Pathological cardiac hypertrophy eventually leads to heart failure without adequate treatment. The immunoproteasome is an inducible form of the proteasome that is intimately involved in inflammatory diseases. Here, we found that the expression and activity of immunoproteasome catalytic subunit β5i were significantly up-regulated in angiotensin II (Ang II)–treated cardiomyocytes and in the hypertrophic hearts. Knockout of β5i in cardiomyocytes and mice markedly attenuated the hypertrophic response, and this effect was aggravated by β5i overexpression in cardiomyocytes and transgenic mice. Mecha

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14

Gibbs, C. L., I. R. Wendt, G. Kotsanas, I. R. Young, and G. Woolley. "Mechanical, energetic, and biochemical changes in long-term pressure overload of rabbit heart." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 3 (1990): H849—H859. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h849.

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The mechanical and energetic consequences of long-term pressure-overload (POL) hypertrophy have been investigated in rabbits and compared with sham-operated controls (SOC). Hypertrophy was induced by banding the pulmonary artery of young rabbits and examining the mechanical, biochemical, and energetic properties of the compensated heart 10-16 wk later. Experiments were undertaken on papillary muscles from the hypertrophic hearts. At 27 degrees C and a stimulus frequency of 1 Hz there was a modest depression of peak stress development but no significant changes in isometric rise times and one-h

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15

Gough, N. R. "Limiting Heart Hypertrophy." Science Signaling 4, no. 165 (2011): ec88-ec88. http://dx.doi.org/10.1126/scisignal.4165ec88.

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16

Trivedi, Chinmay M., and Jonathan A. Epstein. "Heart-Healthy Hypertrophy." Cell Metabolism 13, no. 1 (2011): 3–4. http://dx.doi.org/10.1016/j.cmet.2010.12.012.

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17

Pillai, Jyothish B., Hyde M. Russell, Jai Raman, Valluvan Jeevanandam, and Mahesh P. Gupta. "Increased expression of poly(ADP-ribose) polymerase-1 contributes to caspase-independent myocyte cell death during heart failure." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 2 (2005): H486—H496. http://dx.doi.org/10.1152/ajpheart.00437.2004.

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Poly(ADP-ribose) polymerase-1 (PARP-1) plays a pivotal role in regulating genome stability, cell cycle progression, and cell survival. However, overactivation of PARP has been shown to contribute to cell death and organ failure in various stress-related disease conditions. In this study, we examined the role of PARP in the development and progression of cardiac hypertrophy. We measured the expression of PARP in mouse hearts with physiological (swimming exercise) and pathological (aortic banding) cardiac hypertrophy as well as in human heart samples taken at the time of transplantation. PARP le

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18

Peterson, Erik N., N. Sydney Moise, Cynthia A. Brown, Hollis N. Erb, and Margaret R. Slater. "Heterogeneity of Hypertrophy in Feline Hypertrophic Heart Disease." Journal of Veterinary Internal Medicine 7, no. 3 (1993): 183–89. http://dx.doi.org/10.1111/j.1939-1676.1993.tb03184.x.

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19

Yang, Jin, Xuhui Feng, Qiong Zhou, et al. "Pathological Ace2-to-Ace enzyme switch in the stressed heart is transcriptionally controlled by the endothelial Brg1–FoxM1 complex." Proceedings of the National Academy of Sciences 113, no. 38 (2016): E5628—E5635. http://dx.doi.org/10.1073/pnas.1525078113.

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Genes encoding angiotensin-converting enzymes (Ace and Ace2) are essential for heart function regulation. Cardiac stress enhances Ace, but suppresses Ace2, expression in the heart, leading to a net production of angiotensin II that promotes cardiac hypertrophy and fibrosis. The regulatory mechanism that underlies the Ace2-to-Ace pathological switch, however, is unknown. Here we report that the Brahma-related gene-1 (Brg1) chromatin remodeler and forkhead box M1 (FoxM1) transcription factor cooperate within cardiac (coronary) endothelial cells of pathologically stressed hearts to trigger the Ac

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20

Savchenko, M. I., YU R. Kovalev, and A. P. Kuchinskiy. "HYPERTROPHIC CARDIOMYOPATHY: FIBROSIS OR HYPERTROPHY." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 2 (2013): 148–55. http://dx.doi.org/10.18705/1607-419x-2013-19-2-148-155.

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Objective.Despite the high frequency — 0,2 % (1:500) population, hypertrophic cardiomyopathy (HCM) is still considered one of the most mysterious and misunderstood diseases of myocardium. Insidious pathology has neither specific anatomical and morphological, nor clinical features which makes it a delayed-action bomb: nobody is capable to predict when and what clinical symptoms develop. The clinical phenotype of HCM varies from latent course when the symptoms are absent till rapid progress of heart failure syndrome and sudden cardiac death due to severe arrhythmia. The review covers modern view

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21

Gesmundo, Iacopo, Michele Miragoli, Pierluigi Carullo, et al. "Growth hormone-releasing hormone attenuates cardiac hypertrophy and improves heart function in pressure overload-induced heart failure." Proceedings of the National Academy of Sciences 114, no. 45 (2017): 12033–38. http://dx.doi.org/10.1073/pnas.1712612114.

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It has been shown that growth hormone-releasing hormone (GHRH) reduces cardiomyocyte (CM) apoptosis, prevents ischemia/reperfusion injury, and improves cardiac function in ischemic rat hearts. However, it is still not known whether GHRH would be beneficial for life-threatening pathological conditions, like cardiac hypertrophy and heart failure (HF). Thus, we tested the myocardial therapeutic potential of GHRH stimulation in vitro and in vivo, using GHRH or its agonistic analog MR-409. We show that in vitro, GHRH(1-44)NH2 attenuates phenylephrine-induced hypertrophy in H9c2 cardiac cells, adult

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22

Bingham, A. J., L. Ooi, and I. C. Wood. "Multiple chromatin modifications important for gene expression changes in cardiac hypertrophy." Biochemical Society Transactions 34, no. 6 (2006): 1138–40. http://dx.doi.org/10.1042/bst0341138.

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Cardiac hypertrophy is an increase in the size of cardiac myocytes to generate increased muscle mass, usually driven by increased workload for the heart. Although important during postnatal development and an adaptive response to physical exercise, excessive hypertrophy can result in heart failure. One characteristic of hypertrophy is the re-expression of genes that are normally only expressed during foetal heart development. Although the involvement of these changes in gene expression in hypertrophy has been known for some years, the mechanisms involved in this re-expression are only now bein

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23

Wehbe, Nadine, Suzanne Nasser, Gianfranco Pintus, Adnan Badran, Ali Eid, and Elias Baydoun. "MicroRNAs in Cardiac Hypertrophy." International Journal of Molecular Sciences 20, no. 19 (2019): 4714. http://dx.doi.org/10.3390/ijms20194714.

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Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted g

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Berenji, Kambeez, Mark H. Drazner, Beverly A. Rothermel, and Joseph A. Hill. "Does load-induced ventricular hypertrophy progress to systolic heart failure?" American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (2005): H8—H16. http://dx.doi.org/10.1152/ajpheart.01303.2004.

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Ventricular hypertrophy develops in response to numerous forms of cardiac stress, including pressure or volume overload, loss of contractile mass from prior infarction, neuroendocrine activation, and mutations in genes encoding sarcomeric proteins. Hypertrophic growth is believed to have a compensatory role that diminishes wall stress and oxygen consumption, but Framingham and other studies established ventricular hypertrophy as a marker for increased risk of developing chronic heart failure, suggesting that hypertrophy may have maladaptive features. However, the relative contribution of comor

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Porrello, Enzo R., James R. Bell, Jonathan D. Schertzer, et al. "Heritable pathologic cardiac hypertrophy in adulthood is preceded by neonatal cardiac growth restriction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 3 (2009): R672—R680. http://dx.doi.org/10.1152/ajpregu.90919.2008.

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The identification of genetic factors influencing cardiac growth independently of increased load is crucial to an understanding of the molecular and cellular basis of pathological cardiac hypertrophy. The central aim of this investigation was to determine how pathological hypertrophy in the adult can be linked with disturbances in cardiomyocyte growth and viability in early neonatal development. The hypertrophic heart rat (HHR) model is derived from the spontaneously hypertensive rat and exhibits marked cardiac hypertrophy, in the absence of a pressure load at maturity. Hearts were harvested f

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De Marchi, S. F. "Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function." Heart 83, no. 6 (2000): 678–84. http://dx.doi.org/10.1136/heart.83.6.678.

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27

Li, Yuhao, Yoshihiko Saito, Koichiro Kuwahara, et al. "Guanylyl Cyclase-A Inhibits Angiotensin II Type 2 Receptor-Mediated Pro-Hypertrophic Signaling in the Heart." Endocrinology 150, no. 8 (2009): 3759–65. http://dx.doi.org/10.1210/en.2008-1353.

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Angiotensin II plays a key role in the development of cardiac hypertrophy. The contribution of the angiotensin II type 1 receptor (AT1) in angiotensin II-induced cardiac hypertrophy is well established, but the role of AT2 signaling remains controversial. Previously, we have shown that natriuretic peptide receptor/guanylyl cyclase-A (GCA) signaling protects the heart from hypertrophy at least in part by inhibiting AT1-mediated pro-hypertrophic signaling. Here, we investigated the role of AT2 in cardiac hypertrophy observed in mice lacking GCA. Real-time RT-PCR and immunoblotting approaches ind

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Koga, Kiyokazu, Agnes Kenessey, and Kaie Ojamaa. "Macrophage migration inhibitory factor antagonizes pressure overload-induced cardiac hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 2 (2013): H282—H293. http://dx.doi.org/10.1152/ajpheart.00595.2012.

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Macrophage migration inhibitory factor (MIF) functions as a proinflammatory cytokine when secreted from the cell, but it also exhibits antioxidant properties by virtue of its intrinsic oxidoreductase activity. Since increased production of ROS is implicated in the development of left ventricular hypertrophy, we hypothesized that the redox activity of MIF protects the myocardium when exposed to hemodynamic stress. In a mouse model of myocardial hypertrophy induced by transverse aortic coarctation (TAC) for 10 days, we showed that growth of the MIF-deficient heart was significantly greater by 32

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Roman, Brian B., David L. Geenen, Michael Leitges та Peter M. Buttrick. "PKC-β is not necessary for cardiac hypertrophy". American Journal of Physiology-Heart and Circulatory Physiology 280, № 5 (2001): H2264—H2270. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2264.

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Studies in human and rodent models have shown that activation of protein kinase C-β (PKC-β) is associated with the development of pathological hypertrophy, suggesting that ablation of the PKC-β pathway might prevent or reverse cardiac hypertrophy. To explore this, we studied mice with targeted disruption of the PKC-β gene (knockout, KO). There were no detectable differences in expression or distribution of other PKC isoforms between the KO and control hearts as determined by Western blot analysis. Baseline hemodynamics were measured using a closed-chest preparation and there were no difference

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Gao, Si, Xue-ping Liu, Li-hua Wei, Jing Lu та Peiqing Liu. "Upregulation of α-enolase protects cardiomyocytes from phenylephrine-induced hypertrophy". Canadian Journal of Physiology and Pharmacology 96, № 4 (2018): 352–58. http://dx.doi.org/10.1139/cjpp-2017-0282.

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Cardiac hypertrophy often refers to the abnormal growth of heart muscle through a variety of factors. The mechanisms of cardiomyocyte hypertrophy have been extensively investigated using neonatal rat cardiomyocytes treated with phenylephrine. α-Enolase is a glycolytic enzyme with “multifunctional jobs” beyond its catalytic activity. Its possible contribution to cardiac dysfunction remains to be determined. The present study aimed to investigate the change of α-enolase during cardiac hypertrophy and explore its role in this pathological process. We revealed that mRNA and protein levels of α-eno

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Mavrides, Charalampos, and Borivoj Korecky. "Subcellular distribution of the enzymes of the malate-aspartate shuttle in rat heart and effect of experimental cardiac hypertrophy." Bioscience Reports 5, no. 2 (1985): 95–100. http://dx.doi.org/10.1007/bf01117055.

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The effect of experimental cardiac hypertrophy on the enzymes of the malate – aspartate shuttle aspartate aminotransferase (AAT) and malate dehydrogenase (MDH) was studied. (1) Aortic constriction in adult rats resulted in 25% cardiac hypertrophy in 2½–3 weeks. Total DNA (mg per heart) did not change. (2) The proportions of mitochondrial and cytosolic isozymes of AAT and MDH did not change as a result of cardiac hypertrophy. About two-thirds of each enzyme occurred in the mitochondrial form and one-third in the cytosolic form. (3) Total AAT in hypertrophic hearts, in enzyme units per mg DNA, i

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Ananthasubramaniam, Karthik, Kiran Garikapati, and Celeste T. Williams. "Progressive Left Ventricular Hypertrophy after Heart Transplantation: Insights and Mechanisms Suggested by Multimodal Images." Texas Heart Institute Journal 43, no. 1 (2016): 65–68. http://dx.doi.org/10.14503/thij-14-4657.

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Immunosuppression is the typical measure to prevent rejection after heart transplantation. Although rejection is the usual cause of cardiac hypertrophy, numerous other factors warrant consideration. Calcineurin inhibitors rarely cause hypertrophic cardiomyopathy; the few relevant reports have described children after orthotopic kidney or liver transplantation. We present the case of a 73-year-old woman, an asymptomatic orthotopic heart transplantation patient, in whom chronic immunosuppression with prednisone and cyclosporine apparently caused a phenotype of hypertrophic cardiomyopathy. The na

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Elsherif, Laila, Raymond V. Ortines, Jack T. Saari, and Y. James Kang. "Congestive Heart Failure in Copper-Deficient Mice." Experimental Biology and Medicine 228, no. 7 (2003): 811–17. http://dx.doi.org/10.1177/15353702-0322807-06.

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Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the

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Chung, Eunhee, Fan Yeung, and Leslie A. Leinwand. "Akt and MAPK signaling mediate pregnancy-induced cardiac adaptation." Journal of Applied Physiology 112, no. 9 (2012): 1564–75. http://dx.doi.org/10.1152/japplphysiol.00027.2012.

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Although the signaling pathways underlying exercise-induced cardiac adaptation have been extensively studied, little is known about the molecular mechanisms that result in the response of the heart to pregnancy. The objective of this study was to define the morphological, functional, and gene expression patterns that define the hearts of pregnant mice, and to identify the signaling pathways that mediate this response. Mice were divided into three groups: nonpregnant diestrus control, midpregnancy, and late pregnancy. Both time points of pregnancy were associated with significant cardiac hypert

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Dorn, Lisa E., William Lawrence, Jennifer M. Petrosino, et al. "Microfibrillar-Associated Protein 4 Regulates Stress-Induced Cardiac Remodeling." Circulation Research 128, no. 6 (2021): 723–37. http://dx.doi.org/10.1161/circresaha.120.317146.

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Rationale: Cardiac hypertrophy, a major risk factor for heart failure, occurs when cardiomyocytes remodel in response to complex signaling induced by injury or cell stress. Although cardiomyocytes are the ultimate effectors of cardiac hypertrophy, nonmyocyte populations play a large yet understudied role in determining how cardiomyocytes respond to stress. Objective: To identify novel paracrine regulators of cardiomyocyte hypertrophic remodeling. Methods and Results: We have identified a novel role for a nonmyocyte-derived and TGFβ1 (transforming growth factor β1)–induced extracellular matrix

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Li, Haobo, Lena E. Trager, Xiaojun Liu, et al. "lncExACT1 and DCHS2 Regulate Physiological and Pathological Cardiac Growth." Circulation 145, no. 16 (2022): 1218–33. http://dx.doi.org/10.1161/circulationaha.121.056850.

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Background: The heart grows in response to pathological and physiological stimuli. The former often precedes cardiomyocyte loss and heart failure; the latter paradoxically protects the heart and enhances cardiomyogenesis. The mechanisms underlying these differences remain incompletely understood. Although long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. Methods: RNA sequencing was applied to hearts from mice after 8 weeks of voluntary exercise-induced physiological hypertrophy and c

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Sari, Nurmila, Yasufumi Katanasaka, Hiroki Honda, et al. "Cacao Bean Polyphenols Inhibit Cardiac Hypertrophy and Systolic Dysfunction in Pressure Overload-induced Heart Failure Model Mice." Planta Medica 86, no. 17 (2020): 1304–12. http://dx.doi.org/10.1055/a-1191-7970.

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AbstractPathological stresses such as pressure overload and myocardial infarction induce cardiac hypertrophy, which increases the risk of heart failure. Cacao bean polyphenols have recently gained considerable attention for their beneficial effects on cardiovascular diseases. This study investigated the effect of cacao bean polyphenols on the development of cardiac hypertrophy and heart failure. Cardiomyocytes from neonatal rats were pre-treated with cacao bean polyphenols and then stimulated with 30 µM phenylephrine. C57BL/6j male mice were subjected to sham or transverse aortic constriction

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Ouattara, Alexandre, Olivier Langeron, Rachid Souktani, Stéphane Mouren, Pierre Coriat, and Bruno Riou. "Myocardial and Coronary Effects of Propofol in Rabbits with Compensated Cardiac Hypertrophy." Anesthesiology 95, no. 3 (2001): 699–707. http://dx.doi.org/10.1097/00000542-200109000-00024.

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Background Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. Methods The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and e

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Montiel, Virginie, Ramona Bella, Lauriane Y. M. Michel, et al. "Inhibition of aquaporin-1 prevents myocardial remodeling by blocking the transmembrane transport of hydrogen peroxide." Science Translational Medicine 12, no. 564 (2020): eaay2176. http://dx.doi.org/10.1126/scitranslmed.aay2176.

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Pathological remodeling of the myocardium has long been known to involve oxidant signaling, but strategies using systemic antioxidants have generally failed to prevent it. We sought to identify key regulators of oxidant-mediated cardiac hypertrophy amenable to targeted pharmacological therapy. Specific isoforms of the aquaporin water channels have been implicated in oxidant sensing, but their role in heart muscle is unknown. RNA sequencing from human cardiac myocytes revealed that the archetypal AQP1 is a major isoform. AQP1 expression correlates with the severity of hypertrophic remodeling in

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Zhao, Dingsheng, Guohui Zhong, Jianwei Li, et al. "Targeting E3 Ubiquitin Ligase WWP1 Prevents Cardiac Hypertrophy Through Destabilizing DVL2 via Inhibition of K27-Linked Ubiquitination." Circulation 144, no. 9 (2021): 694–711. http://dx.doi.org/10.1161/circulationaha.121.054827.

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Background: Without adequate treatment, pathological cardiac hypertrophy induced by sustained pressure overload eventually leads to heart failure. WWP1 (WW domain–containing E3 ubiquitin protein ligase 1) is an important regulator of aging-related pathologies, including cancer and cardiovascular diseases. However, the role of WWP1 in pressure overload–induced cardiac remodeling and heart failure is yet to be determined. Methods: To examine the correlation of WWP1 with hypertrophy, we analyzed WWP1 expression in patients with heart failure and mice subjected to transverse aortic constriction (T

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McLennan, Peter L., Mahinda Y. Abeywardena, Julie A. Dallimore, and Daniel Raederstorff. "Dietary fish oil preserves cardiac function in the hypertrophied rat heart." British Journal of Nutrition 108, no. 4 (2011): 645–54. http://dx.doi.org/10.1017/s0007114511005915.

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Regular fish or fish oil intake is associated with a low incidence of heart failure clinically, and fish oil-induced reduction in cardiac remodelling seen in hypertrophy models may contribute. We investigated whether improved cardiac energy efficiency in non-hypertrophied hearts translates into attenuation of cardiac dysfunction in hypertrophied hearts. Male Wistar rats (n 33) at 8 weeks of age were sham-operated or subjected to abdominal aortic stenosis to produce pressure-overload cardiac hypertrophy. Starting 3 weeks post-operatively to follow initiation of hypertrophy, rats were fed a diet

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Haenen, N. "Lipomatous hypertrophy of the interatrial septum." Heart 88, no. 1 (2002): 111. http://dx.doi.org/10.1136/heart.88.1.111.

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Johansson, Markus, Benyapa Tangruksa, Sepideh Heydarkhan-Hagvall, Anders Jeppsson, Peter Sartipy, and Jane Synnergren. "Data Mining Identifies CCN2 and THBS1 as Biomarker Candidates for Cardiac Hypertrophy." Life 12, no. 5 (2022): 726. http://dx.doi.org/10.3390/life12050726.

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Cardiac hypertrophy is a condition that may contribute to the development of heart failure. In this study, we compare the gene-expression patterns of our in vitro stem-cell-based cardiac hypertrophy model with the gene expression of biopsies collected from hypertrophic human hearts. Twenty-five differentially expressed genes (DEGs) from both groups were identified and the expression of selected corresponding secreted proteins were validated using ELISA and Western blot. Several biomarkers, including CCN2, THBS1, NPPA, and NPPB, were identified, which showed significant overexpressions in the h

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Ruzicka, M., and F. H. Leenen. "Renin-angiotensin system and minoxidil-induced cardiac hypertrophy in rats." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (1993): H1551—H1556. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1551.

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Besides cardiac volume overload, cardiac sympathetic activity and the renin-angiotensin system (RAS) are activated by arterial vasodilators such as minoxidil. To evaluate the possible involvement of the RAS in the development of minoxidil-induced cardiac hypertrophy, we assessed in normotensive rats minoxidil-induced changes in cardiac and plasma renin activity (PRA) and the potential of chronic treatment with the angiotensin-converting enzyme (ACE) inhibitor enalapril and the nonpeptide angiotensin II receptor blocker losartan to prevent minoxidil-induced cardiac hypertrophy. PRA increased in

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Zeitz, Michael J., and James W. Smyth. "Translating Translation to Mechanisms of Cardiac Hypertrophy." Journal of Cardiovascular Development and Disease 7, no. 1 (2020): 9. http://dx.doi.org/10.3390/jcdd7010009.

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Cardiac hypertrophy in response to chronic pathological stress is a common feature occurring with many forms of heart disease. This pathological hypertrophic growth increases the risk for arrhythmias and subsequent heart failure. While several factors promoting cardiac hypertrophy are known, the molecular mechanisms governing the progression to heart failure are incompletely understood. Recent studies on altered translational regulation during pathological cardiac hypertrophy are contributing to our understanding of disease progression. In this brief review, we describe how the translational m

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Frey, Norbert, Hugo A. Katus, Eric N. Olson, and Joseph A. Hill. "Hypertrophy of the Heart." Circulation 109, no. 13 (2004): 1580–89. http://dx.doi.org/10.1161/01.cir.0000120390.68287.bb.

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Nicholls, M. G. "Hypertension, hypertrophy, heart failure." Heart 76, no. 3 Suppl 3 (1996): 92–97. http://dx.doi.org/10.1136/hrt.76.3_suppl_3.92.

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Zhang, Haifeng, Shanshan Li, Qiulian Zhou, et al. "Qiliqiangxin Attenuates Phenylephrine-Induced Cardiac Hypertrophy through Downregulation of MiR-199a-5p." Cellular Physiology and Biochemistry 38, no. 5 (2016): 1743–51. http://dx.doi.org/10.1159/000443113.

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Background/Aims: Qiliqiangxin (QL), a traditional Chinese medicine, has long been used to treat chronic heart failure. Previous studies demonstrated that QL could prevent cardiac remodeling and hypertrophy in response to hypertensive or ischemic stress. However, little is known about whether QL could modulate cardiac hypertrophy in vitro, and (if so) whether it is through modulation of specific hypertrophy-related microRNA. Methods: The primary neonatal rat ventricular cardiomyocytes were isolated, cultured, and treated with phenylephrine (PE, 50 µmol/L, 48 h) to induce hypertrophy in vitro, i

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Liao, Hai-han, Nan Zhang, Yan-yan Meng, et al. "Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6/TAK1/MAPK and Nrf2 Signaling Pathway." Oxidative Medicine and Cellular Longevity 2019 (December 6, 2019): 1–14. http://dx.doi.org/10.1155/2019/6304058.

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Myricetin (Myr) is a common plant-derived polyphenol and is well recognized for its multiple activities including antioxidant, anti-inflammation, anticancer, and antidiabetes. Our previous studies indicated that Myr protected mouse heart from lipopolysaccharide and streptozocin-induced injuries. However, it remained to be unclear whether Myr could prevent mouse heart from pressure overload-induced pathological hypertrophy. Wild type (WT) and cardiac Nrf2 knockdown (Nrf2-KD) mice were subjected to aortic banding (AB) surgery and then administered with Myr (200 mg/kg/d) for 6 weeks. Myr signific

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Xu, Man, Run-Qing Xue, Yi Lu, et al. "Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway." Cardiovascular Research 115, no. 3 (2018): 530–45. http://dx.doi.org/10.1093/cvr/cvy217.

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Abstract Aims Cardiac hypertrophy is characterized by a shift in metabolic substrate utilization, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline. Methods and results The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats. Cardiomyocyte size and cardiac fibrosis were significantly increased in hypertrophic hearts. In vitro cardiomyoc

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