Autophagy and pressure overload-induced cardiac hypertrophy

Zeng, Yong; Wen, Ai-Zhen; Zhang, Wen; Fan, Fuyuan; Chen, Ou-Ying

doi:10.1080/10286020.2021.2024810

Cited by 2 publications

(2 citation statements)

References 48 publications

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“…34,51 Basal level of autophagy can clear damaged organelles and misfolded proteins to maintain cell homeostasis and protect cardiomyocyte against endotoxin. 52,53 Enhancing level of autophagy in response to certain conditions, such as hypoxia, starvation, and stress stimuli, can promote survival. 54,55 Some studies found that LPS-induced autophagy serves as a cytoprotective role during sepsis and activation of autophagy could repress LPS-induced cell toxicity and thus protect against septic cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

Xing,

Gao,

Bai

et al. 2024

Journal of Cardiovascular Pharmacology

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Sepsis-induced cardiac dysfunction represents a major cause of high mortality in intensive care units with limited therapeutic options. Golgi protein 73 (GP73) has been implicated in various diseases. However, the role of GP73 in LPS-induced cardiac dysfunction is unclear. Here, we established sepsis-induced cardiac dysfunction model by LPS administration in wild type (WT) and GP73 knockout (GP73 -/- ) mice. We found GP73 was increased in LPS-treated mouse hearts and LPS-cultured neonatal rat cardiomyocytes (NRCMs). Knockout of GP73 alleviated myocardial injury and improved cardiac dysfunction. Moreover, depletion of GP73 in NRCMs relieved LPS-induced cardiomyocyte apoptosis and activated myocardial autophagy. Therefore, GP73 is a negative regulator in LPS-induced cardiac dysfunction by promoting cardiomyocyte apoptosis and inhibiting cardiomyocyte autophagy.

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Section: Discussionmentioning

confidence: 99%

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

Xing,

Gao,

Bai

et al. 2024

Journal of Cardiovascular Pharmacology

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“…Cardiac hypertrophy, an early pathological change in heart failure, is a response to increased load-induced ventricular wall pressure to maintain cardiac output and persistent myocardial hypertrophy eventually leads to decompensation 3,4 . There are many reasons for myocardial hypertrophy, such as angiotensin II 5 , stress-induced 6 or mediated by certain chemical substances 7 . Some adipokines are independent risk factors for cardiac hypertrophy 8,9 .…”

Section: Introductionmentioning

confidence: 99%

Resistin Induces Cardiomyocyte Hypertrophy in H9c2 Embryonic Rat Myocardial Cells via Inhibition of MiR-489-3p

Yang,

Hao,

et al. 2023

Trends Med. Res

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Background and Objective:The miRNAs play an important regulatory role in resistin-induced cardiac hypertrophy. The purpose of this experiment was to investigate the effect of resistin-induced myocardial hypertrophy in H9c2 cardiomyocytes by inhibiting the expression of miR-489-3p. Materials and Methods: After treatment with resistin or resistin plus miR-489-3p mimic, Image J was used to measure cell surface area. The BCA method and cell counting were used to measure protein synthesis. RT-qPCR was used to measure the relative expression levels of atrial natriuretic factor (ANF), brain natriuretic factor (BNF) and miR-489-3p. Results: Overexpression of the miR-489-3p reduced resistin-induced increase in cardiomyocyte area. Overexpression of miR-489-3p attenuated protein synthesis induced by resistin. Overexpression of miR-489-3p decreased the relative expression of cardiac hypertrophy marker ANF and BNF increased by resistin. Resistin inhibited the expression of miR-489-3p. Conclusion:Resistin induces cardiomyocyte hypertrophy by inhibiting the expression of miR-489-3p. This study provides a theoretical basis for further research on the role of miRNA in resistin-induced cardiomyocyte hypertrophy.

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Autophagy and pressure overload-induced cardiac hypertrophy

Cited by 2 publications

References 48 publications

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

Resistin Induces Cardiomyocyte Hypertrophy in H9c2 Embryonic Rat Myocardial Cells via Inhibition of MiR-489-3p

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