Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China.
Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, 510515, Guangzhou, China.
Heart Fail Rev. 2024 Jan;29(1):113-123. doi: 10.1007/s10741-023-10354-x. Epub 2023 Oct 12.
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.
心力衰竭的进展据报道与心肌细胞中的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脏功能障碍。反过来,异常自噬又会损害线粒体功能,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,形成一个恶性循环,使心力衰竭恶化。然而,线粒体功能障碍和异常自噬之间的相互作用在心力衰竭发展中的作用仍然不清楚,其潜在机制主要难以捉摸。线粒体功能障碍和异常自噬之间的联系在心力衰竭进展中的潜在作用最近引起了关注。本综述总结了心力衰竭发展过程中线粒体和自噬之间相互作用的最新进展。