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解析线粒体间的相互作用:心力衰竭发病机制的新前沿。

Unraveling mitochondrial crosstalk: a new frontier in heart failure pathogenesis.

作者信息

Chang Hongbo, He Pingge, Liu Weidi, Wu Hong, Wang Zhentao

机构信息

Second School of Clinical Medicine, Henan University of Chinese Medicine, Zhengzhou, China.

Department of Cardiovascular Medicine, Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.

出版信息

Front Cardiovasc Med. 2025 Jul 15;12:1641023. doi: 10.3389/fcvm.2025.1641023. eCollection 2025.

Abstract

Mitochondria play a central role in energy production and signal transduction in cardiomyocytes. Their dysfunction is a key contributor to the development and progression of heart failure (HF). Beyond energy metabolism, mitochondria regulate calcium homeostasis, autophagy, protein synthesis, lipid metabolism, and gene expression through close interactions with other organelles. Disruption of these interactions has been linked to HF pathophysiology.This review focuses on the dynamic communication between mitochondria and five major organelles-the endoplasmic reticulum, lysosomes, ribosomes, lipid droplets, and the nucleus. We outline how these interactions maintain cardiac homeostasis and describe how their dysfunction contributes to HF. We also highlight emerging therapeutic strategies targeting these organelle networks.

摘要

线粒体在心肌细胞的能量产生和信号转导中起着核心作用。其功能障碍是心力衰竭(HF)发生和发展的关键因素。除能量代谢外,线粒体通过与其他细胞器的密切相互作用来调节钙稳态、自噬、蛋白质合成、脂质代谢和基因表达。这些相互作用的破坏与HF的病理生理学有关。本综述重点关注线粒体与五种主要细胞器——内质网、溶酶体、核糖体、脂滴和细胞核之间的动态通讯。我们概述了这些相互作用如何维持心脏稳态,并描述了它们的功能障碍如何导致HF。我们还强调了针对这些细胞器网络的新兴治疗策略。

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Mitochondrial non-energetic function and embryonic cardiac development.线粒体的非能量功能与胚胎心脏发育
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