Abstract 309: Small Heterodimer Partner Blocks Cardiac Hypertrophy By Interfering With GATA6 Signaling

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yoon Seok Nam ◽  
Duk-Hwa Kwon ◽  
Gwang Hyeon Eom ◽  
Hyun Kook
Keyword(s):  
Cardiac Hypertrophy ◽  
Heart Diseases ◽  
Cardiomyocyte Hypertrophy ◽  
Physical Interaction ◽  
Orphan Nuclear Receptor ◽  
Promoter Regions ◽  
Adult Heart ◽  
Hypertrophic Response ◽  
Small Heterodimer Partner

Rationale: Small heterodimer partner (SHP; NR0B2) is an atypical orphan nuclear receptor that lacks a conventional DNA binding domain. By interacting with other transcription factors, SHP regulates diverse biological events including glucose metabolism in liver. The role of SHP in adult heart diseases has not yet been demonstrated. Objective: We aimed to investigate the role of SHP in adult heart in association with cardiac hypertrophy. Methods and Results: The roles of SHP in cardiac hypertrophy were tested in primary cultured cardiomyocytes and in animal models. SHP null mice showed a hypertrophic phenotype. Hypertrophic stresses repressed the expression of SHP, whereas forced expression of SHP blocked the development of cardiomyocyte hypertrophy. SHP reduced the protein amount of Gata6. By direct physical interaction with Gata6, SHP interfered with the binding of Gata6 to GATA binding elements in the promoter regions of natriuretic peptide precursor type A. Metformin, an anti-diabetic agent, induced SHP and suppressed cardiac hypertrophy. The metformin-induced anti-hypertrophic effect was attenuated either by SHP siRNA in cardiomyocytes or in SHP null mice. Conclusions: These results establish SHP as a novel anti-hypertrophic regulator that acts by interfering with GATA6 signaling. SHP may participate in the metformin-induced anti-hypertrophic response.

P4999Cardiomyocyte ErbB4 receptors are essential for developmental cardiac hypertrophy and cardiac function in adult hearts

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Reichelt ◽  
Z Wang ◽  
C Thorn ◽  
T Paravicini ◽  
W G Thomas
Keyword(s):  
Cardiac Hypertrophy ◽  
Dilated Cardiomyopathy ◽  
Heart Development ◽  
Contractile Function ◽  
Critical Role ◽  
Tamoxifen Treatment ◽  
Cardiomyocyte Hypertrophy ◽  
Adult Heart ◽  
Neonatal Mice

Abstract Background/Introduction Activation of ErbB4 by neuregulin 1 (NRG1) promotes cardiomyocyte hypertrophy and proliferation in both adult and neonatal mice, while treatment of patients with NRG1 following myocardial infarction reduces scar size and improves function. In mice, deletion of ErbB4 from cardiomyocytes mid-gestation results in development of dilated cardiomyopathy and reduced survival, pointing to a critical role for ErbB4 in the heart. Purpose We sought to evaluate the role of ErbB4 in the adult heart. Methods and results We deleted ErbB4 in αMHC-MerCreMer (cCre Tg+/)/ErbB4 homozygote floxed (ErbB4 fl/fl) mice at ∼2 months of age with 10 injections of Tamoxifen (20 mg/kg/day). Contractile function was reduced in vivo (echocardiography, 16%) and ex vivo (isolated-perfused, 33%) 3 months after gene deletion, while survival in mice up to 8 months after tamoxifen treatment was mot modified by cardiomyocyte ErbB4 deletion. We next evaluated the role of ErbB4 in response to physiological and pathological hypertrophic stressors. ErbB4 deletion did not modify cardiac enlargement in response to Angiotensin II (1000ng/kg/min, 14 days) or exercise (twice daily swimming, 20 min/session increasing 10 min/day to 90 min followed by 7 days at 90 min/session). Taken together, this indicated that ErbB4 is not essential for survival and adaptation in the adult heart, pointing instead towards a critical window for ErbB4 in neonatal heart development. To test this hypothesis, ErbB4ff and ErbB4ww neonates were injected at P1 with AAV9-cTNT-eGFP-iCre (2.16x1011viral particles, temporal vein) and culled at P6. We confirmed the presence of iCre mRNA, and suppression of ErbB4 in ErbB4 ff/ff mice, coincident with increased NRG1a, and reduced body and ventricular weights. By day 28, a number of hearts showed evidence of dilated cardiomyopathy. Conclusion Thus, ErbB4 is critical to cardiac hypertrophy and growth in neonatal mice, and maintains adult heart function. Acknowledgement/Funding National Health and Medical Research Council

scholarly journals Corosolic acid ameliorates cardiac hypertrophy via regulating autophagy

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Zhao-Peng Wang ◽  
Difei Shen ◽  
Yan Che ◽  
Ya-Ge Jin ◽  
Sha-Sha Wang ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
In Vivo Studies ◽  
Cardiomyocyte Hypertrophy ◽  
H9c2 Cells ◽  
Hypertrophic Response ◽  
Post Surgery ◽  
Corosolic Acid

Abstract Aim: In this work, we explored the role of corosolic acid (CRA) during pressure overload-induced cardiac hypertrophy. Methods and results: Cardiac hypertrophy was induced in mice by aortic banding. Four weeks post-surgery, CRA-treated mice developed blunted cardiac hypertrophy, fibrosis, and dysfunction, and showed increased LC3 II and p-AMPK expression. In line with the in vivo studies, CRA also inhibited the hypertrophic response induced by PE stimulation accompanying with increased LC3 II and p-AMPK expression. It was also found that CRA blunted cardiomyocyte hypertrophy and promoted autophagy in Angiotensin II (Ang II)-treated H9c2 cells. Moreover, to further verify whether CRA inhibits cardiac hypertrophy by the activation of autophagy, blockade of autophagy was achieved by CQ (an inhibitor of the fusion between autophagosomes and lysosomes) or 3-MA (an inhibitor of autophagosome formation). It was found that autophagy inhibition counteracts the protective effect of CRA on cardiac hypertrophy. Interestingly, AMPK knockdown with AMPKα2 siRNA-counteracted LC3 II expression increase and the hypertrophic response inhibition caused by CRA in PE-treated H9c2 cells. Conclusion: These results suggest that CRA may protect against cardiac hypertrophy through regulating AMPK-dependent autophagy.

Abstract 282: Role of a Disintegrin and Metalloproteinase 15 in Cardiac Hypertrophy and Fibrosis Following Pressure Overload

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Priya Aujla ◽  
Sayantan Jana ◽  
Michael Chute ◽  
Zamaneh Kassiri
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Fibrosis ◽  
Cell Function ◽  
Systolic Function ◽  
Mechanical Strain ◽  
Pressure Overload ◽  
Compensatory Hypertrophy ◽  
Hypertrophic Response ◽  
A Disintegrin And Metalloproteinase

Introduction: Disintegrin and metalloproteinases (ADAMs) are membrane-bound cell surface enzymes that are capable of both proteolytic functions (via the metalloproteinase domain) and adhesive functions (via the disintegrin domain), whereby they can influence cell function and extracellular matrix (ECM) remodelling in the heart. ADAM15 is unique among the ADAMs, as it is also capable of degrading ECM proteins. ADAM12 and ADAM17 have been reported to regulate cardiac hypertrophy, but the role of ADAM15 in cardiac hypertrophy is not known. This study investigates the role of ADAM15 in cardiac hypertrophy and fibrosis following pressure overload. Methods & Results: Genetically modified male ADAM15-deficient ( Adam15 -/- ) and wildtype (WT) mice were subjected to cardiac pressure overload by transverse aortic constriction (TAC). Cardiac function and structural remodelling were assessed using echocardiography at 2-, and 6-wks post-TAC. Hearts were excised at 2-, or 6-wks post-TAC. Adam15 -/- hearts presented greater hypertrophy and decreased cardiac systolic function at 6wks post-TAC, but no difference at 2wks post-TAC compared to WT-TAC mice. Adam15 -/- hearts also showed exacerbated fibrosis at 6wks post-TAC, but not at 2wks post-TAC, compared to WT. Mechanical strain (i.e. pressure overload) triggers two temporally activated pathways leading to an initial compensatory hypertrophy, which can culminate to decompensation and dilated cardiomyopathy. Consistent with the greater hypertrophy, phosphorylation of ERK1/2, JNK1/2/3, and GSK3β was increased in Adam15 -/- mice. The calcineurin-NFAT pathways can mediate pressure overload-induced hypertrophy, but we found that Adam15-deficiency did not impact this pathway. The mechanism responsible for this function of ADAM15 requires further investigation. Conclusion: This study reports a novel cardioprotective function for ADAM15 in pressure overload, where loss of ADAM15 promotes cardiac fibrosis and decompensated cardiac hypertrophy but does not alter the compensated hypertrophic response.

scholarly journals SGK1-Sensitive Regulation of Cyclin-Dependent Kinase Inhibitor 1B (p27) in Cardiomyocyte Hypertrophy

2015 ◽  
Vol 37 (2) ◽  
pp. 603-614 ◽  
Author(s):  
Jakob Voelkl ◽  
Tatsiana Castor ◽  
Katharina Musculus ◽  
Robert Viereck ◽  
Sobuj Mia ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Kinase Inhibitor ◽  
Protein Localization ◽  
Phosphorylation Site ◽  
Cardiomyocyte Hypertrophy ◽  
Mrna Levels ◽  
Cyclin Dependent Kinase ◽  
Transcript Levels ◽  
Hypertrophic Response ◽  
Cyclin Dependent Kinase Inhibitor

Background/Aims: The serum- and glucocorticoid-inducible kinase SGK1 participates in the orchestration of cardiac hypertrophy and remodeling. Signaling linking SGK1 activity to cardiac remodeling is, however, incompletely understood. SGK1 phosphorylation targets include cyclin-dependent kinase inhibitor 1B (p27), a protein which suppresses cardiac hypertrophy. The present study explored how effects of SGK1 on nuclear p27 localization might modulate the hypertrophic response in cardiomyocytes. Methods: Experiments were performed in HL-1 cardiomyocytes and in SGK1-deficient (sgk1-/-) and corresponding wild-type (sgk1+/+) mice following pressure overload by transverse aortic constriction (TAC). Transcript levels were quantified by RT-PCR, protein abundance by Western blotting and protein localization by confocal microscopy. Results: In HL-1 cardiomyocytes, overexpression of constitutively active SGK1 (SGK1S422D) but not of inactive SGK1 (SGK1K127N) increased significantly the cell size and transcript levels encoding Acta1, a molecular marker of hypertrophy. Those effects were paralleled by almost complete relocation of p27 in the cytoplasm. Treatment of HL-1 cardiomyocytes with isoproterenol was followed by up-regulation of SGK1 expression. Moreover, isoproterenol treatment stimulated the hypertrophic response and was followed by disappearance of p27 from the nuclei, effects prevented by the SGK1 inhibitor EMD638683. The effect of SGK1S422D overexpression on Acta1 mRNA levels was disrupted by overexpression of p27 and of the p27T197A mutant lacking the SGK1 phosphorylation site, but not of the phosphomimetic p27T197D mutant. In sgk1+/+ mice, TAC increased significantly SGK1 and Acta1 mRNA levels and decreased the nuclear to cytoplasmic protein ratio of p27 in cardiac tissue, effects blunted in the sgk1-/- mice. Conclusion: SGK1-induced hypertrophy of cardiomyocytes involves p27 phosphorylation at T197, which fosters cytoplasmic p27 localization.

scholarly journals Role of CyPA in cardiac hypertrophy and remodeling

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Mengfei Cao ◽  
Wei Yuan ◽  
Meiling Peng ◽  
Ziqi Mao ◽  
Qianru Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Interstitial Fibrosis ◽  
Systolic Function ◽  
Cardiac Fibroblasts ◽  
Cardiomyocyte Hypertrophy ◽  
Pathological Cardiac Hypertrophy ◽  
Complex Process

Abstract Pathological cardiac hypertrophy is a complex process and eventually develops into heart failure, in which the heart responds to various intrinsic or external stress, involving increased interstitial fibrosis, cell death and cardiac dysfunction. Studies have shown that oxidative stress is an important mechanism for this maladaptation. Cyclophilin A (CyPA) is a member of the cyclophilin (CyPs) family. Many cells secrete CyPA to the outside of the cells in response to oxidative stress. CyPA from blood vessels and the heart itself participate in a variety of signaling pathways to regulate the production of reactive oxygen species (ROS) and mediate inflammation, promote cardiomyocyte hypertrophy and proliferation of cardiac fibroblasts, stimulate endothelial injury and vascular smooth muscle hyperplasia, and promote the dissolution of extracellular matrix (ECM) by activating matrix metalloproteinases (MMPs). The events triggered by CyPA cause a decline of diastolic and systolic function and finally lead to the occurrence of heart failure. This article aims to introduce the role and mechanism of CyPA in cardiac hypertrophy and remodeling, and highlights its potential role as a disease biomarker and therapeutic target.

Abstract 541: Dyxin/Lmcd1, A Novel LIM Protein, Is Both Necessary And Sufficient For The Induction Of Cardiomyocyte Hypertrophy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Derk Frank ◽  
Christiane Hanselmann ◽  
Rainer Will ◽  
Hugo A Katus ◽  
Norbert Frey
Keyword(s):  
Cardiac Hypertrophy ◽  
Molecular Mechanisms ◽  
Mrna Level ◽  
Neonatal Rat ◽  
Cardiomyocyte Hypertrophy ◽  
Rat Cardiomyocytes ◽  
Hypertrophic Response ◽  
Lim Protein ◽  
A Genome ◽  
Necessary And Sufficient

Sustained cardiac hypertrophy may lead to heart failure and sudden death. While significant progress has been made in elucidating the underlying molecular mechanisms, it is believed that several molecules that modulate cardiomyocyte growth remain elusive. To identify novel candidates involved in hypertrophic signalling, we conducted a genome-wide screening experiment by subjecting neonatal rat cardiomyocytes (NRCM) to either biomechanical stretch or phenylephrine (PE) stimulation followed by microarray analyses. Among several other molecules (stretch: n=164; PE: n=238), the new LIM protein Dyxin/Lmcd1 was significantly upregulated both by stretch (5.6fold, p<0.001) and PE (2.5 fold, p<0.01). Moreover, Dyxin was markedly induced in hypertrophic hearts of transgenic mice overexpressing the phosphatase calcineurin (3.8fold on mRNA- and 2.9fold on protein level (both p<0.01)). To dissect the putative function of this novel molecule, we adenovirally overexpressed Dyxin in NRCM, which led to marked cellular hypertrophy (1.5fold increase in cell surface area, p<0.001) and induction of ANF (3.8fold, p<0.05). In addition, the calcineurin-responsive gene MCIP1.4 was found upregulated (3.2fold, p<0.001), suggesting that Dyxin activates the calcineurin pathway. In order to test whether Dyxin is also required for cardiomyocyte hypertrophy, we stimulated NRCVM with either PE or stretch and utilized adenovirus-encoded microRNAs to knock down Dyxin (−75% on protein, −85% on mRNA level). While both PE and stretch induced significant hypertrophy (+41% and +48%, p<0.001), the inhibition of Dyxin expression completely blunted the hypertrophic response to both stimuli (p<0.001). Consistently, induction of the “hypertrophic gene program” (including ANF, BNP, and alpha-skeletal actin) was abrogated. Likewise, PE-mediated upregulation of MCIP1.4 expression (7.3fold; p<0.001), was entirely prevented by the knockdown of Dyxin (0.8fold, p=n.s.). We show here that Dyxin, which has not been implicated in hypertrophy before, is significantly upregulated in cardiac hypertrophy. Moreover, it is both necessary and sufficient for cardiomyocyte hypertrophy, and this effect is mediated, at least in part by modulation of calcineurin signalling.

Abstract 17: MicroRNA-30c Modulates Diabetes-Induced Cardiac Hypertrophy via PI3K/Akt Signaling Pathway

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Satish K Raut ◽  
Akhilesh Kumar ◽  
Gurinder B Singh ◽  
Rajni Sharma ◽  
Uma Saikia ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Tissue ◽  
Signalling Pathway ◽  
Cardiomyocyte Hypertrophy ◽  
Control Group ◽  
Cardiac Tissues ◽  
Mhc Genes ◽  
Altered Gene ◽  
And Control

Cardiomyocyte hypertrophy leading to cardiac failure is one of the characteristic alterations in Diabetic Cardiomyopathy. Several regulatory mechanisms mediate altered gene expression in DCM. Alterations in several myocardial miRs have been demonstrated in cardiac hypertrophy but the role of miR-30c in the pathophysiology of diabetes induced cardiac hypertrophy is not known. Objective: miR-30c may be involved in modulating expression of key genes (Rac1, Cdc42 and Pak1) of PI3K/Akt signalling pathway involved in cardiac hypertrophy in DCM. Method: DCM was induced in Wistar rats by STZ-high fat diet combination and animals were sacrificed after 12 weeks of diabetes. The expression of miR-30c, Rac1, Cdc42 and Pak1 genes and markers of hypertrophy (ANP and β-MHC) was studied in cardiac tissues (n=6) and control rats (n=6) by qRT-PCR. Result: We observed 4 fold increased expression of ANP and 2.2 fold of β-MHC genes in DCM group as compared to control group (n=6) (p<0.05). Decreased expression of miR-30c (3.3 fold) was seen in DCM model at 12 weeks compared to control group (n=6) (p<0.05). Expression of three specific targets of miR-30c i.e. Cdc42, Pak1, and Rac1, regulating cardiac hypertrophy, was found to be significantly increased by 1.94 fold, 1.8 fold, and 1.2 fold in cardiac tissues of DCM model respectively and was inversely related to miR-30c expression. Conclusion: Our results suggest that down regulation of miR-30c in cardiac tissue may play a key role in regulation of diabetes associated cardiac hypertrophy by modulating PI3K/Akt signalling pathway.

Abstract 434: Sirt4 Accelerates Ang II-induced Pathological Cardiac Hypertrophy by Inhibiting Mnsod Activity

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Depei Liu ◽  
Yu-Xuan Luo ◽  
Xiaoqiang Tang ◽  
Xi-Zhou An ◽  
Xue-Min Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transgenic Mice ◽  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Manganese Superoxide Dismutase ◽  
Ang Ii ◽  
Hypertrophic Response ◽  
Hypertrophic Growth ◽  
Pathological Cardiac Hypertrophy

Aims: Oxidative stress contributes to the development of cardiac hypertrophy and heart failure. One of the mitochondrial sirtuins, Sirt4, is highly expressed in the heart, but its function remains unknown. The aim of the present study was to investigate the role of Sirt4 in the pathogenesis of pathological cardiac hypertrophy and the molecular mechanism by which Sirt4 regulates mitochondrial oxidative stress. Methods and results: Male C57BL/6 Sirt4 knockout mice, transgenic mice exhibiting cardiac-specific overexpression of Sirt4 (Sirt4-Tg) and their respective controls were treated with angiotensin II (Ang II). At 4 weeks, hypertrophic growth of cardiomyocytes, fibrosis and cardiac function were analyzed. Sirt4 deficiency conferred resistance to Ang II infusion by significantly suppressing hypertrophic growth, and the deposition of fibrosis. In Sirt4-Tg mice, aggravated hypertrophy and reduced cardiac function were observed compared with non-transgenic mice following Ang II treatment. Mechanistically, Sirt4 inhibited the binding of manganese superoxide dismutase (MnSOD) to Sirt3, another member of the mitochondrial sirtuins, and increased MnSOD acetylation levels to reduce its activity, resulting in elevated reactive oxygen species (ROS) accumulation upon Ang II stimulation. Furthermore, inhibition of ROS with MnTBAP, a mimetic of SOD, blocked the Sirt4-mediated aggravation of the hypertrophic response in Ang II-treated Sirt4-Tg mice. Conclusions: Sirt4 promotes hypertrophic growth and cardiac dysfunction by increasing ROS levels upon pathological stimulation. These findings reveal a role of Sirt4 in pathological cardiac hypertrophy, providing a new potential therapeutic strategy for this disease.

scholarly journals PRMT7 Ablation in Cardiomyocytes Causes Cardiac Hypertrophy and Fibrosis Through β-Catenin Dysregulation

2021 ◽  
Author(s):  
Byeong-Yun Ahn ◽  
Myong-Ho Jeong ◽  
Jung-Hoon Pyun ◽  
Hyeon-Ju Jeong ◽  
Tuan Anh Vuong ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Wnt Signaling Pathway ◽  
Rat Cardiomyocytes ◽  
Hypertrophic Response ◽  
Cellular Hypertrophy ◽  
Pathway Inhibition ◽  
Normal Cardiac Function ◽  
Inhibitor Treatment

Abstract Angiotensin II (AngII) has potent cardiac hypertrophic effects mediated through activation of hypertrophic signaling like Wnt/b-Catenin signaling. In the current study, we examined the role of protein arginine methyltransferase 7 (PRMT7) in cardiac function. PRMT7 was greatly decreased in hypertrophic hearts chronically infused with AngII and cardiomyocytes treated with AngII. PRMT7 depletion in rat cardiomyocytes resulted in hypertrophic responses. Consistently, mice lacking PRMT7 exhibited displayed the cardiac hypertrophy and fibrosis. PRMT7 overexpression abrogated the cellular hypertrophy elicited by AngII, while PRMT7 depletion exacerbated the hypertrophic response caused by AngII. Similar with AngII treatment, the cardiac transcriptome analysis of PRMT7-deficient hearts revealed the alteration in gene expression profile related to Wnt signaling pathway. Inhibition of PRMT7 by gene deletion or an inhibitor treatment enhanced the activity of b-Catenin. PRMT7 deficiency decreases symmetric dimethylation of b-Catenin. Mechanistic studies reveal that methylation of arginine residue 93 in b-Catenin decreases the activity of b-Catenin. Taken together, our data suggest that PRMT7 is important for normal cardiac function through suppression of b-Catenin activity.

scholarly journals Osteoprotegerin prompts cardiomyocyte hypertrophy via FAK/BECLIN1 mediated autophagy inhibition

2019 ◽  
Author(s):  
anna shen ◽  
Dezhong Zheng ◽  
Tingrong Liu ◽  
Tao Zhou
Keyword(s):  
Inflammatory Factors ◽  
Cardiomyocyte Hypertrophy ◽  
Rat Cardiomyocytes ◽  
Immunoprecipitation Assay ◽  
Hypertrophic Response ◽  
Cellular Hypertrophy ◽  
Si Rna ◽  
Autophagy Inhibition ◽  
Cultured Cardiomyocytes

Abstract Aim It has been reported that Osteoprotegerin (OPG) induces cardiomyocyte hypertrophy, but the mechanism remains unclear. This study was to investigate the role of Focal Adhesion Kinase (FAK) pathway in the OPG induced hypertrophy in cultured cardiomyocytes.Methods The H9C2 line of rat cardiomyocytes were treated with OPG at different concentrations and the cellular hypertrophy was evaluated. Meanwhile, the activity of FAK and other the phosphorylation kinases were detected. Autophagy flux assay was performed in absence and presence OPG. The interaction between proteins was analyses using Co-Immunoprecipitation assay.Results We found that OPG induced cardiomyocyte hypertrophic response, accompanied by dramatic increases a series of inflammatory factors and cytokines, as well as collagen synthesis. Also OPG inhibits autophagy and induces FAK phosphorylation. FAK silencing using si-RNA abrogates the effect of OPG on autophagy and cellular hypertrophy. Furthermore, Co-Immunoprecipitation assay reveals that OPG inhibits autophagy through enhancing the binding of FAK and Beclin1 Tyr 233.Conclusion The FAK/Beclin1 signal pathway is essential for the OPG induced autophagy inhibition and hypertrophic response in cultured H9C2 cells.

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