Autophagy protects mitochondrial health in heart failure
Autophagy protects mitochondrial health in heart failure
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DOI：
10.1007/s10741-023-10354-x
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发表时间：
2023-10-12
影响因子：
4.6
通讯作者：
Chen，Yanmei
中科院分区：
文献类型：
--
作者：
Tang，Yating;Xu，Wenlong;Chen，Yanmei
据报道，心力衰竭的进展与心肌细胞内稳态失衡密切相关，如线粒体功能障碍和异常自噬。线粒体功能障碍引发自噬和心功能障碍。反过来，异常的自噬损害线粒体功能，并在某些情况下导致细胞凋亡或自噬性细胞死亡。这些事件通常同时发生，形成恶性循环，加重心力衰竭。然而，线粒体功能障碍和异常自噬之间的串扰在心力衰竭的发展中的作用仍然不清楚，其潜在机制主要是难以捉摸的。线粒体功能障碍和异常自噬在心力衰竭进展中的潜在作用最近引起了人们的关注。本文就心力衰竭发生发展过程中线粒体与自噬相互作用的研究进展作一综述。
The progression of heart failure is reported to be strongly associated with homeostatic imbalance, such as mitochondrial dysfunction and abnormal autophagy, in the cardiomyocytes. Mitochondrial dysfunction triggers autophagic and cardiac dysfunction. In turn, abnormal autophagy impairs mitochondrial function and leads to apoptosis or autophagic cell death under certain circumstances. These events often occur concomitantly, forming a vicious cycle that exacerbates heart failure. However, the role of the crosstalk between mitochondrial dysfunction and abnormal autophagy in the development of heart failure remains obscure and the underlying mechanisms are mainly elusive. The potential role of the link between mitochondrial dysfunction and abnormal autophagy in heart failure progression has recently garnered attention. This review summarized recent advances of the interactions between mitochondria and autophagy during the development of heart failure.