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塑造心脏命运:翻译后修饰在内质网-线粒体串扰对心脏重塑中的作用

Shaping cardiac destiny: the role of post-translational modifications on endoplasmic reticulum - mitochondria crosstalk in cardiac remodeling.

作者信息

Zhang Xiaohan, Shi Shuqing, Du Yihang, Chai Ruoning, Guo Zezhen, Duan Chenglin, Wang Huan, Hu Yuanhui, Chang Xing, Du Bai

机构信息

Department of Cardiology, Guang'Anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Department of Internal Medicine, Guang'Anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

出版信息

Front Pharmacol. 2024 Oct 11;15:1423356. doi: 10.3389/fphar.2024.1423356. eCollection 2024.

DOI:10.3389/fphar.2024.1423356
PMID:39464632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11502351/
Abstract

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.

摘要

心脏重构是大多数心血管疾病共有的病理变化。它既包括适应性生理反应,也包括失代偿性病理变化。在解剖学上,心房重构主要由心房颤动引起,而心室重构通常由心肌梗死、高血压或心肌病诱发。线粒体作为心肌细胞的动力源,与内质网等其他细胞器协同作用,以控制多种病理生理过程,如钙信号传导、脂质转运、线粒体动力学、生物发生和线粒体自噬。这一机制已被证明对心脏重构至关重要。翻译后修饰可通过调节蛋白质功能、稳定性和相互作用来调控心脏细胞内的信号通路、基因表达和细胞应激反应,从而塑造心肌对损伤和应激的反应。这些修饰,特别是磷酸化、乙酰化和泛素化,对于调节构成心脏重构基础的复杂分子途径至关重要。本综述全面概述了心脏重构过程中内质网与线粒体之间的相互作用,重点关注各种翻译后修饰对这些相互作用的调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75fb/11502351/0192ca66cfe3/fphar-15-1423356-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75fb/11502351/fbab0d074015/fphar-15-1423356-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75fb/11502351/0192ca66cfe3/fphar-15-1423356-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75fb/11502351/fbab0d074015/fphar-15-1423356-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75fb/11502351/0192ca66cfe3/fphar-15-1423356-g002.jpg

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