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REVIEW article

Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1423356
This article is part of the Research Topic Mitochondria Interact With the Endoplasmic Reticulum for Myocardium Injury and Vascular Endothelial Injury Under Stress: Pathological and Targeted Therapy View all 4 articles

Shaping Cardiac Destiny: The Role of Post-translational Modifications on Endoplasmic Reticulum -Mitochondria Crosstalk in Cardiac Remodeling

Provisionally accepted
  • 1 Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China
  • 2 Macquarie University, Sydney, New South Wales, Australia

The final, formatted version of the article will be published soon.

    Cardiac remodeling is a shared pathological change in most cardiovascular diseases. encompassing both adaptive physiological responses and decompensated pathological changes. Anatomically, atrial remodeling is primarily caused by atrial fibrillation, whereas ventricular remodeling is typically induced by myocardial infarction, hypertension, or cardiomyopathy. Mitochondria, the powerhouse of cardiomyocytes, collaborate with other organelles such as the endoplasmic reticulum to control a variety of pathophysiological processes such as calcium signaling, lipid transfer, mitochondrial dynamics, biogenesis, and mitophagy. This mechanism is proven to be essential for cardiac remodeling. Post-translational modifications can regulate intracellular signaling pathways, gene expression, and cellular stress responses in cardiac cells by modulating protein function, stability, and interactions, consequently shaping the myocardial response to injury and stress. These modifications, in particular phosphorylation, acetylation, and ubiquitination, are essential for the regulation of the complex molecular pathways that underlie cardiac remodeling. This review provides a comprehensive overview of the crosstalk between the endoplasmic reticulum and mitochondria during cardiac remodeling, focusing on the regulatory effects of various post-translational modifications on these interactions.

    Keywords: Cardiac Remodeling1, Post-translational Modifications2, Endoplasmic Reticulum -Mitochondria Crosstalk3, Chronic Heart Failure4, Atrial Fibrillation keyword5

    Received: 26 Apr 2024; Accepted: 23 Sep 2024.

    Copyright: © 2024 ZHANG, 杜, Chai, Shi, Guo, Duan, Wang, Hu, Chang and Du. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Zezhen Guo, Macquarie University, Sydney, 2109, New South Wales, Australia
    Huan Wang, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China
    Yuanhui Hu, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China
    Xing Chang, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China
    Bai Du, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.