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Journal articles on the topic 'Hypertrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Maron, Barry J., and Carolyn Y. Ho. "Hypertrophic Cardiomyopathy Without Hypertrophy." JACC: Cardiovascular Imaging 2, no. 1 (2009): 65–68. http://dx.doi.org/10.1016/j.jcmg.2008.09.008.

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2

Strøm, Claes C., Mogens Kruhøffer, Steen Knudsen, et al. "Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy." Comparative and Functional Genomics 5, no. 6-7 (2004): 459–70. http://dx.doi.org/10.1002/cfg.428.

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Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved in h

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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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Lu, Peilei, Danyu Zhang, Fan Ding, Jialu Ma, Yang K. Xiang, and Meimi Zhao. "Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis." Cells 12, no. 12 (2023): 1667. http://dx.doi.org/10.3390/cells12121667.

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Pathological cardiac hypertrophy is one of the notable causes of heart failure. Circular RNAs (circRNAs) have been studied in association with cardiac hypertrophy; however, the mechanisms by which circRNAs regulate cardiac hypertrophy remain unclear. In this study, we identified a new circRNA, named circCacna1c, in cardiac hypertrophy. Adult male C57BL/6 mice and H9c2 cells were treated with isoprenaline hydrochloride (ISO) to establish a hypertrophy model. We found that circCacna1c was upregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. Western blot and quantitative real-time

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Abdelbaki, Mourad, A. Boureghda, and N. Hanifi. "Comparative Research Between Sportsman's Heart and Hypertrophic Cardiomyopathy." International Journal of Innovative Research in Medical Science 9, no. 01 (2024): 24–27. http://dx.doi.org/10.23958/ijirms/vol09-i01/1802.

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Physiological left ventricular hypertrophy is the result of the left ventricle having to function harder due to intense physical exercise. After exercise is stopped, this modest and reversible hypertrophy persists. Studying these structural alterations is now feasible because to cardiac echodoppler. Distinguishing this adaptive hypertrophy from the pathogenic hypertrophic cardiomyopathy might be challenging at times. We examined 212 athletes who competed and a group of hypertrophic cardiomyopathy patients who had asymmetric septal hypertrophy that was confirmed. The findings demonstrated that

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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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Morita, Kozo, Takeshi Miyamoto, Nobuyuki Fujita, et al. "Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification." Journal of Experimental Medicine 204, no. 7 (2007): 1613–23. http://dx.doi.org/10.1084/jem.20062525.

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Chondrocyte hypertrophy during endochondral ossification is a well-controlled process in which proliferating chondrocytes stop proliferating and differentiate into hypertrophic chondrocytes, which then undergo apoptosis. Chondrocyte hypertrophy induces angiogenesis and mineralization. This step is crucial for the longitudinal growth and development of long bones, but what triggers the process is unknown. Reactive oxygen species (ROS) have been implicated in cellular damage; however, the physiological role of ROS in chondrogenesis is not well characterized. We demonstrate that increasing ROS le

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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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9

Ignatenko, G. I., G. G. Taradin, and T. E. Kugler. "Specifics of Left Ventricular Hypertrophy and Characteristic of Phenotypic Variants in Patients with Hypertrophic Cardiomyopathy." Russian Archives of Internal Medicine 13, no. 4 (2023): 282–93. http://dx.doi.org/10.20514/2226-6704-2023-13-4-282-293.

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Hypertrophic cardiomyopathy is characterized by genetic and phenotypic heterogeneity which manifests in different variants of localization and extent of myocardial hypertrophy.Aim: to evaluate specifics of left ventricular hypertrophy, the prevalence and characteristics of clinical and instrumental features of phenotypic variants of hypertrophic cardiomyopathy.Materials and methods. The study includes 295 patients with hypertrophic cardiomyopathy aged 18 to 88 years (60.3±13.4 years), 183 men (62 %), and women 112 (38 %). The diagnosis of which was established by 2D echocardiography. The sever

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Villeneuve, C., A. Caudrillier, C. Ordener, N. Pizzinat, A. Parini, and J. Mialet-Perez. "Dose-dependent activation of distinct hypertrophic pathways by serotonin in cardiac cells." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 2 (2009): H821—H828. http://dx.doi.org/10.1152/ajpheart.00345.2009.

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There is substantial evidence supporting a hypertrophic action of serotonin [5-hydroxytryptamine (5-HT)] in cardiomyocytes. However, little is known about the mechanisms involved. We previously demonstrated that 5-HT-induced hypertrophy depends, in part, on the generation of reactive oxygen species by monoamine oxidase-A (MAO-A) (see Ref. 3 ). Cardiomyocytes express 5-HT2 receptors, which may also participate in hypertrophy. Here, we analyzed the respective contribution of 5-HT2 receptors and MAO-A in H9C2 cardiomyoblast hypertrophy. 5-HT induced a dose-dependent increase in [3H]leucine incorp

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Olimovna, Oripova Ozoda. "CHARACTERISTICS OF PATHOMORPHOLOGICAL CHANGES IN HYPERTROPHIC CARDIOMYOPATHY." American Journal Of Biomedical Science & Pharmaceutical Innovation 4, no. 6 (2024): 70–78. http://dx.doi.org/10.37547/ajbspi/volume04issue06-10.

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In hypertrophic cardiomyopathy, the walls of the ventricles of the heart continue with symmetric or asymmetric myocardial hypertrophy. Morphologically, in hypertrophic cardiomyopathy, fibrotic foci are detected based on the incorrect arrangement of myocardial muscle fibers, small coronary vessel syndrome, and myocardial hypertrophy.

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Li, Yingxiao, Chao-Tien Hsu, Ting-Ting Yang, and Kai-Chun Cheng. "Syringaldehyde Alleviates Cardiac Hypertrophy Induced by Hyperglycemia in H9c2 Cells Through GLP-1 Receptor Signals." Pharmaceuticals 18, no. 1 (2025): 110. https://doi.org/10.3390/ph18010110.

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Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA’s therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. Methods: H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertro

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Raghunathan, Suchi, Ramesh K. Goyal, and Bhoomika M. Patel. "Selective inhibition of HDAC2 by magnesium valproate attenuates cardiac hypertrophy." Canadian Journal of Physiology and Pharmacology 95, no. 3 (2017): 260–67. http://dx.doi.org/10.1139/cjpp-2016-0542.

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The regulatory paradigm in cardiac hypertrophy involves alterations in gene expression that is mediated by chromatin remodeling. Various data suggest that class I and class II histone deacetylases (HDACs) play opposing roles in the regulation of hypertrophic pathways. To address this, we tested the effect of magnesium valproate (MgV), an HDAC inhibitor with 5 times more potency on class I HDACs. Cardiac hypertrophy was induced by partial abdominal aortic constriction in Wistar rats, and at the end of 6 weeks, we evaluated hypertrophic, hemodynamic, and oxidative stress parameters, and mitochon

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Riedl, Moritz, Christina Witzmann, Matthias Koch, et al. "Attenuation of Hypertrophy in Human MSCs via Treatment with a Retinoic Acid Receptor Inverse Agonist." International Journal of Molecular Sciences 21, no. 4 (2020): 1444. http://dx.doi.org/10.3390/ijms21041444.

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In vitro chondrogenically differentiated mesenchymal stem cells (MSCs) have a tendency to undergo hypertrophy, mirroring the fate of transient “chondrocytes” in the growth plate. As hypertrophy would result in ossification, this fact limits their use in cartilage tissue engineering applications. During limb development, retinoic acid receptor (RAR) signaling exerts an important influence on cell fate of mesenchymal progenitors. While retinoids foster hypertrophy, suppression of RAR signaling seems to be required for chondrogenic differentiation. Therefore, we hypothesized that treatment of cho

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15

Nikkholgh, Ahad, Fatemeh Tavakoli, Nasrin Alborzi, and Fatemeh Araste. "Vitamin D Attenuates Cardiac Hypertrophy in Rats through mRNA Regulation of Interleukin-6 and Its Receptor." Research in Cardiovascular Medicine 12, no. 4 (2023): 123–28. http://dx.doi.org/10.4103/rcm.rcm_60_23.

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Abstract Context: Interleukin-6 (IL-6), a pro-inflammatory cytokine, plays an important role in the pathogenesis of myocardial hypertrophy. By integrating its membrane receptor complex (gp80), IL-6 activates the signal guidance components (gp130) and activates the hypertrophic signaling pathways. There is some evidence that 1,25 dihydroxyvitamin D exerts antihypertrophic effects, but the cellular and molecular mechanisms are not fully understood. The aim of this study was to evaluate the effect of calcitriol on the level of IL-6 and its receptor components in hypertrophied rat heart. Subjects

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Yan, Xiaoying, Ran Zhao, Xiaorong Feng та ін. "Sialyltransferase7A promotes angiotensin II-induced cardiomyocyte hypertrophy via HIF-1α-TAK1 signalling pathway". Cardiovascular Research 116, № 1 (2019): 114–26. http://dx.doi.org/10.1093/cvr/cvz064.

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Abstract Aims Sialylation is up-regulated during the development of cardiac hypertrophy. Sialyltransferase7A (Siat7A) mRNA is consistently over-expressed in the hypertrophic left ventricle of hypertensive rats independently of genetic background. The aims of this study were: (i) to detect the Siat7A protein levels and its roles in the pathological cardiomyocyte hypertrophy; (ii) to elucidate the effect of sialylation mediated by Siat7A on the transforming-growth-factor-β-activated kinase (TAK1) expression and activity in cardiomyocyte hypertrophy; and (iii) to clarify hypoxia-inducible factor

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Nosenko, N. M., D. V. Shchehlov, M. Yu Mamonova, and Ya E. Kudelskyi. "Left ventricular hypertrophy: differential diagnosis." Endovascular Neuroradiology 30, no. 4 (2020): 49–58. http://dx.doi.org/10.26683/2304-9359-2019-4(30)-49-58.

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There are some imaging methods for the diagnosis of left ventricular hypertrophy. Such as echocardiography, computed tomography, magnetic resonance imaging. These methods help to identify changes at different stages, evaluate the prognosis, stratify the risk and differential diagnosis.The left ventricle hypertrophy is a condition that may be due to physiological adaptation due to overload. For example, in patients with arterial hypertension, in athletes, and so on. Left ventricle hypertrophy may also be associated with a change in the actual structure: for example, with hypertrophic cardiomyop

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Bazgir, Farhad, Julia Nau, Saeideh Nakhaei-Rad, et al. "The Microenvironment of the Pathogenesis of Cardiac Hypertrophy." Cells 12, no. 13 (2023): 1780. http://dx.doi.org/10.3390/cells12131780.

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Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial

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Gallo, Simona, Annapia Vitacolonna, Alessandro Bonzano, Paolo Comoglio, and Tiziana Crepaldi. "ERK: A Key Player in the Pathophysiology of Cardiac Hypertrophy." International Journal of Molecular Sciences 20, no. 9 (2019): 2164. http://dx.doi.org/10.3390/ijms20092164.

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Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detrimental stimuli. Nevertheless, long-term stimuli incite chronic hypertrophy and may lead to heart failure. In this review, we analyze the recent literature regarding the role of ERK (extracellular signal-regulated kinase) activity in cardiac hypertrophy. ERK signaling produces beneficial effects during the early phase of chronic pressure overload in response to G protein-coupled receptors (GPCRs) and integrin stimulation. These functions comprise (i) adaptive concentric hypertrophy and (ii) cell

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Su, Dongmei, Sun Jing, Lina Guan, et al. "Role of Nodal–PITX2C signaling pathway in glucose-induced cardiomyocyte hypertrophy." Biochemistry and Cell Biology 92, no. 3 (2014): 183–90. http://dx.doi.org/10.1139/bcb-2013-0124.

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Pathological cardiac hypertrophy is a major cause of morbidity and mortality in cardiovascular disease. Recent studies have shown that cardiomyocytes, in response to high glucose (HG) stimuli, undergo hypertrophic growth. While much work still needs to be done to elucidate this important mechanism of hypertrophy, previous works have showed that some pathways or genes play important roles in hypertrophy. In this study, we showed that sublethal concentrations of glucose (25 mmol/L) could induce cardiomyocyte hypertrophy with an increase in the cellular surface area and the upregulation of the at

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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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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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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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Li, Yu, Bo He, Chao Zhang, Yanji He, Tianyang Xia, and Chunyu Zeng. "Naringenin Attenuates Isoprenaline-Induced Cardiac Hypertrophy by Suppressing Oxidative Stress through the AMPK/NOX2/MAPK Signaling Pathway." Nutrients 15, no. 6 (2023): 1340. http://dx.doi.org/10.3390/nu15061340.

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Cardiac hypertrophy is accompanied by increased myocardial oxidative stress, and whether naringenin, a natural antioxidant, is effective in the therapy of cardiac hypertrophy remains unknown. In the present study, different dosage regimens (25, 50, and 100 mg/kg/d for three weeks) of naringenin (NAR) were orally gavaged in an isoprenaline (ISO) (7.5mg/kg)-induced cardiac hypertrophic C57BL/6J mouse model. The administration of ISO led to significant cardiac hypertrophy, which was alleviated by pretreatment with naringenin in both in vivo and in vitro experiments. Naringenin inhibited ISO-induc

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Liu, Yang, Shuang Li, Zhanqun Gao, et al. "Indoleamine 2,3-Dioxygenase 1 (IDO1) Promotes Cardiac Hypertrophy via a PI3K-AKT-mTOR-Dependent Mechanism." Cardiovascular Toxicology 21, no. 8 (2021): 655–68. http://dx.doi.org/10.1007/s12012-021-09657-y.

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AbstractIndoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme for tryptophan metabolism, involved in immune cell differentiation/maturation and cancer biology. IDO1 is also expressed in cardiomyocytes, but its roles in the cardiovascular system are not fully understood. Here, we reported the functions of IDO1 during cardiac hypertrophy. Quantitative real-time PCR and Western blot experiments demonstrated the upregulation of IDO1 mRNA and protein levels in human and hypertrophic mouse hearts, as well as in angiotensin II (Ang II)-induced hypertrophic rat cardiomyocytes. IDO1 activity and metabolite

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Hernández Quiles, C., and L. M. Beltrán Romero. "Hypertrophic cardiomyopathy: Beyond left ventricular hypertrophy." Revista Clínica Española (English Edition) 221, no. 6 (2021): 343–44. http://dx.doi.org/10.1016/j.rceng.2020.03.005.

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SUN, XUE-FENG, QING-JUN WU, YA-LAN BI, et al. "Primary Hypertrophic Osteoarthropathy with Gastric Hypertrophy." Journal of Rheumatology 38, no. 5 (2011): 959–60. http://dx.doi.org/10.3899/jrheum.101077.

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Silver, Meredith M., and Malcolm D. Silver. "Left ventricular hypertrophy versus hypertrophic cardlomyopathy." Journal of Pediatrics 121, no. 3 (1992): 500–501. http://dx.doi.org/10.1016/s0022-3476(05)81824-4.

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Borer, Jeffrey S. "Left ventricular hypertrophy in hypertrophic cardiomyopathy." Journal of the American College of Cardiology 44, no. 2 (2004): 406–8. http://dx.doi.org/10.1016/j.jacc.2004.04.023.

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Tang, Xin, Lihong Pan, Shuang Zhao, et al. "SNO-MLP (S-Nitrosylation of Muscle LIM Protein) Facilitates Myocardial Hypertrophy Through TLR3 (Toll-Like Receptor 3)–Mediated RIP3 (Receptor-Interacting Protein Kinase 3) and NLRP3 (NOD-Like Receptor Pyrin Domain Containing 3) Inflammasome Activation." Circulation 141, no. 12 (2020): 984–1000. http://dx.doi.org/10.1161/circulationaha.119.042336.

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Background: S-nitrosylation (SNO), a prototypic redox-based posttranslational modification, is involved in the pathogenesis of cardiovascular disease. The aim of this study was to determine the role of SNO of MLP (muscle LIM protein) in myocardial hypertrophy, as well as the mechanism by which SNO-MLP modulates hypertrophic growth in response to pressure overload. Methods: Myocardial samples from patients and animal models exhibiting myocardial hypertrophy were examined for SNO-MLP level using biotin-switch methods. SNO sites were further identified through liquid chromatography–tandem mass sp

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Liu, Yao-Lung, Chiu-Ching Huang, Chiz-Chung Chang, et al. "Hyperphosphate-Induced Myocardial Hypertrophy through the GATA-4/NFAT-3 Signaling Pathway Is Attenuated by ERK Inhibitor Treatment." Cardiorenal Medicine 5, no. 2 (2015): 79–88. http://dx.doi.org/10.1159/000371454.

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Background/Aims: Numerous epidemiological studies have associated elevated serum phosphorus levels with cardiovascular disease and the risk of death in the general population as well as in chronic kidney disease (CKD) and dialysis patients. In this study, we explored whether elevated phosphate conditions induce cardiac hypertrophy and attempted to identify the molecular and cellular mechanisms in the hypertrophic response. Methods: H9c2 myocardial cells were incubated in high-phosphate conditions to induce hypertrophy. Pathological hypertrophic responses were measured in terms of cell size, ar

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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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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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Goodman, Craig A., Man Hing Miu, John W. Frey, et al. "A Phosphatidylinositol 3-Kinase/Protein Kinase B-independent Activation of Mammalian Target of Rapamycin Signaling Is Sufficient to Induce Skeletal Muscle Hypertrophy." Molecular Biology of the Cell 21, no. 18 (2010): 3258–68. http://dx.doi.org/10.1091/mbc.e10-05-0454.

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It has been widely proposed that signaling by mammalian target of rapamycin (mTOR) is both necessary and sufficient for the induction of skeletal muscle hypertrophy. Evidence for this hypothesis is largely based on studies that used stimuli that activate mTOR via a phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB)-dependent mechanism. However, the stimulation of signaling by PI3K/PKB also can activate several mTOR-independent growth-promoting events; thus, it is not clear whether signaling by mTOR is permissive, or sufficient, for the induction of hypertrophy. Furthermore, the presum

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Preveden, Andrej, Mirna Usorac, Mirko Todic, Mihaela Preveden, Miodrag Golubovic, and Lazar Velicki. "Electrocardiographic features of patients with hypertrophic cardiomyopathy." Medical review 75, no. 1-2 (2022): 56–61. http://dx.doi.org/10.2298/mpns2202056p.

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Introduction. Hypertrophic cardiomyopathy is a disorder of the myocardium characterized by asymmetric or symmetric left ventricular hypertrophy. It is often an inherited disorder with an autosomal dominant pattern. The aim of this study was to evaluate the electrocardiographic characteristics of patients with hypertrophic cardiomyopathy, as well as to assess the accuracy of current electrocardiographic criteria for left ventricular hypertrophy used as indicators of hypertrophic cardiomyopathy. Material and Methods. This retrospective study was conducted using hospital medical records of 42 pat

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Prinz, Christian, Lothar Faber, Dieter Horstkotte, et al. "Evaluation of left ventricular torsion in children with hypertrophic cardiomyopathy." Cardiology in the Young 24, no. 2 (2013): 245–52. http://dx.doi.org/10.1017/s104795111300005x.

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AbstractAimsTo evaluate the role of torsion in hypertrophic cardiomyopathy in children.MethodsA total of 88 children with idiopathic hypertrophic cardiomyopathy (n = 24) and concentric hypertrophy (n = 20) were investigated with speckle-tracking echocardiography and compared with age- and gender-matched healthy controls (n = 44).ResultsIn hypertrophic cardiomyopathy, we found increased torsion (2.8 ± 1.6 versus 1.9 ± 1.0°/cm [controls], p < 0.05) because of an increase in clockwise basal rotation (−8.7 ± 4.3° versus −4.9 ± 2.5° [controls], p < 0.001) and prolonged time to peak diastolic

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Khatoon, Razia, Swaimanti Sarkar, Aindrila Chattopadhyay, and Debasish Bandyopadhyay. "The cardioprotective potential of melatonin on cardiac hypertrophy: A mechanistic overview." Melatonin Research 6, no. 3 (2023): 313–44. http://dx.doi.org/10.32794/mr112500157.

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Cardiac hypertrophy (CH) is an increment of muscle mass to maintain the heart regular operations. A physiological cardiac hypertrophy due to exercise or other normal physiological process is characterized by normal contractile function and structural framework of heart tissue. In contrast, pathological hypertrophy occurs in response to increased pressure or volume overload from several cardiovascular diseases including hypertension, valvular diseases, cardiac infarction and heart failure. It is of major concern as it is one of the leading causes of death worldwide. Despite much progress in thi

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Quddus, Sharmin, Tapati Mandal, Sharmin Reza, et al. "SPECT Myocardial Perfusion Imaging in the Diagnosis of Apical Hypertrophic Cardiomyopathy- Case Series and Literature Review." Bangladesh Journal of Nuclear Medicine 27, no. 1 (2024): 100–106. http://dx.doi.org/10.3329/bjnm.v27i1.71520.

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Apical hypertrophic cardiomyopathy (AHCM) is a subtype of hypertrophic cardiomyopathy (HCM) in which hypertrophy mostly affects the apex of the left ventricle, resulting in mid-ventricular obstruction. The diagnosis is usually made when the LV apex has an apical wall thickness of ≥ 15 mm in echocardiography, though sometimes it is missed due to the poor acoustic window in two-dimensional echocardiography. Single Photon Emission Computed Tomography-Myocardial Perfusion Imaging (SPECT-MPI) can often detect apical hypertrophy. The apical hypertrophy was identified by SPECT-MPI in the reported thr

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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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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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Luo, Dan, Jueyan Wang, Shijiao Zheng та ін. "Crocin ameliorates hypertension-induced cardiac hypertrophy and apoptosis by activating AMPKα signalling". Clinical and Investigative Medicine 48, № 1 (2025): 11–23. https://doi.org/10.3138/cim-2024-0118.

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Purpose Cardiac hypertrophy is a critical contributor to heart failure. Therapies that effectively manage cardiac hypertrophy are still inadequate. Crocin is a natural component of saffron, and its beneficial properties have been previously documented. This study aimed to investigate the role of crocin in cardiac hypertrophy and apoptosis and its related mechanisms. Methods Sprague-Dawley rats were infused with angiotensin II (Ang II; 520 ng/kg/min) or normal saline and then intraperitoneally injected with crocin (40 mg/kg) or dimethyl sulfoxide for 4 weeks. Systolic and diastolic blood pressu

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Lysova, I. V., and T. P. Senatorova. "Treatment of hypertrophic gingivitis with laser radiation." Kazan medical journal 69, no. 2 (1988): 122. http://dx.doi.org/10.17816/kazmj97214.

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The treatment of hypertrophic gingivitis in adolescence is difficult and often accompanied by recurrences. There are recommendations on the exposure mode of the helium-neon laser, which inhibits cell proliferation with a photosensitizer, for the treatment of chronic hypertrophic gingivitis. We studied the efficacy of laser therapy in juvenile gingivitis. We treated 10 patients aged 16 to 18 years with the edematous form of hypertrophic gingivitis. Four of them had grade I hypertrophy of gingival papillae and six had grade II hypertrophy.

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Wang, Yao-Sheng, Jing Zhou, Kui Hong, Xiao-Shu Cheng, and Yi-Gang Li. "MicroRNA-223 Displays a Protective Role Against Cardiomyocyte Hypertrophy by Targeting Cardiac Troponin I-Interacting Kinase." Cellular Physiology and Biochemistry 35, no. 4 (2015): 1546–56. http://dx.doi.org/10.1159/000373970.

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Background/Aims: MicroRNAs play regulatory role in cardiovascular disease. MicroRNA-223 (miR-223) was found to be expressed abundantly in myocardium. TNNI3K, a novel cardiac troponin I (cTnI)-interacting and cardiac hypertrophy related kinase, is computationally predicted as a potential target of miR-223. This study was designed to investigate the cellular and molecular effects of miR-223 on cardiomyoctye hypertrophy, focusing on the role of TNNI3K. Methods: Neonatal rat cardiomyocytes (CMs) were cultured, and CMs hypertrophy was induced by endothelin-1 (ET-1). In vivo cardiac hypertrophy was

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Geraets, Ilvy M. E., Will A. Coumans, Agnieszka Strzelecka, et al. "Metabolic Interventions to Prevent Hypertrophy-Induced Alterations in Contractile Properties In Vitro." International Journal of Molecular Sciences 22, no. 7 (2021): 3620. http://dx.doi.org/10.3390/ijms22073620.

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(1) Background: The exact mechanism(s) underlying pathological changes in a heart in transition to hypertrophy and failure are not yet fully understood. However, alterations in cardiac energy metabolism seem to be an important contributor. We characterized an in vitro model of adrenergic stimulation-induced cardiac hypertrophy for studying metabolic, structural, and functional changes over time. Accordingly, we investigated whether metabolic interventions prevent cardiac structural and functional changes; (2) Methods: Primary rat cardiomyocytes were treated with phenylephrine (PE) for 16 h, 24

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Brown, Brittany F., Anita Quon, Jason R. B. Dyck, and Joseph R. Casey. "Carbonic anhydrase II promotes cardiomyocyte hypertrophy." Canadian Journal of Physiology and Pharmacology 90, no. 12 (2012): 1599–610. http://dx.doi.org/10.1139/y2012-142.

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Pathological cardiac hypertrophy, the maladaptive remodelling of the myocardium, often progresses to heart failure. The sodium–proton exchanger (NHE1) and chloride–bicarbonate exchanger (AE3) have been implicated as important in the hypertrophic cascade. Carbonic anhydrase II (CAII) provides substrates for these transporters (protons and bicarbonate, respectively). CAII physically interacts with NHE1 and AE3, enhancing their respective ion transport activities by increasing the concentration of substrate at their transport sites. Earlier studies found that a broad-spectrum carbonic anhydrase i

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Li, Peng-Long, Hui Liu, Guo-Peng Chen, et al. "STEAP3 (Six-Transmembrane Epithelial Antigen of Prostate 3) Inhibits Pathological Cardiac Hypertrophy." Hypertension 76, no. 4 (2020): 1219–30. http://dx.doi.org/10.1161/hypertensionaha.120.14752.

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Pathological cardiac hypertrophy is one of the major predictors and inducers of heart failure, the end stage of various cardiovascular diseases. However, the molecular mechanisms underlying pathogenesis of pathological cardiac hypertrophy remain largely unknown. Here, we provided the first evidence that STEAP3 (Six-Transmembrane Epithelial Antigen of Prostate 3) is a key negative regulator of this disease. We found that the expression of STEAP3 was reduced in pressure overload-induced hypertrophic hearts and phenylephrine-induced hypertrophic cardiomyocytes. In a transverse aortic constriction

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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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Meng, Chen, Haibi Su, Meiling Shu, et al. "The functional role of m6A demethylase ALKBH5 in cardiomyocyte hypertrophy." Cell Death & Disease 15, no. 9 (2024). http://dx.doi.org/10.1038/s41419-024-07053-2.

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AbstractCardiomyocyte hypertrophy is a major outcome of pathological cardiac hypertrophy. The m6A demethylase ALKBH5 is reported to be associated with cardiovascular diseases, whereas the functional role of ALKBH5 in cardiomyocyte hypertrophy remains confused. We engineered Alkbh5 siRNA (siAlkbh5) and Alkbh5 overexpressing plasmid (Alkbh5 OE) to transfect cardiomyocytes. Subsequently, RNA immunoprecipitation (RIP)-qPCR, MeRIP-qPCR analysis and the dual-luciferase reporter assays were applied to elucidate the regulatory mechanism of ALKBH5 on cardiomyocyte hypertrophy. Our study identified ALKB

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Guedes de Sousa, Caio, José Maria Del Castillo, Carlos Mazzarollo, et al. "Comparative Analysis of the Coronary Arteries Flow Pattern in Secondary Myocardial Hypertrophies and by Sarcomeric Mutation." ABC Imagem Cardiovascular 34, no. 1 (2021). http://dx.doi.org/10.47593/2675-312x/20213401eabc131.

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Background: Coronary flow with a diastolic predominance increases two to five times in hyperemia, mediated by vasodilation (coronary flow reserve, CFR) and, in hypertrophy, relative ischemia may occur. In secondary hypertrophy (LVH), the flow, normal at rest, becomes ischemic due to increased demand. In hypertrophic cardiomyopathy (HCM) with perivascular fibrosis, collateral vessels appear to increase the irrigation of hypertrophied segments. Objective: To determine the coronary flow pattern in patients with secondary hypertrophy and hypertrophic cardiomyopathy,evaluating the coronary flow res

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Fang, Jiajin, and Shuai Wang. "Bibliometric analysis of research trends and emerging insights of osteoarthritis and chondrocyte hypertrophy." Frontiers in Surgery 12 (April 10, 2025). https://doi.org/10.3389/fsurg.2025.1538339.

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BackgroundThis study aims to systematically analyze the intersection of OA and chondrocyte hypertrophy using bibliometric methods, providing an quantitative and comprehensive overview of the current research status and emerging trends in this field.MethodsRelevant publications were retrieved from the Web of Science Core Collection database using the search query TS = (“chondrocyte* hypertroph*” OR “hypertrophic chondrocyte*” OR “cartilage hypertroph*”) AND (“osteoarthriti*” OR “OA” OR “degenerative arthritis”). Several bibliometric tools, including Vosviewer, CiteSpace, the R package (bibliome

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