Laboratory of Heart Valve Disease, West China Hospital, Sichuan University, 37 Guoxue Street, Chengdu 610064, China.
Department of Cardiology, West China Hospital, Sichuan University, 37 Guoxue Street, Chengdu 610064, China.
Oxid Med Cell Longev. 2022 Sep 27;2022:2849985. doi: 10.1155/2022/2849985. eCollection 2022.
The pathological mechanisms underlying cardiac remodelling and cardiac dysfunction caused by pressure overload are poorly understood. Mitochondrial damage and functional dysfunction, including mitochondrial bioenergetic disorder, oxidative stress, and mtDNA damage, contribute to heart injury caused by pressure overload. Mitophagy, an important regulator of mitochondrial homeostasis and function, is triggered by mitochondrial damage and participates in the pathological process of cardiovascular diseases. Recent studies indicate that mitophagy plays a critical role in the pressure overload model, but evidence on the causal relationship between mitophagy abnormality and pressure overload-induced heart injury is inconclusive. This review summarises the mechanism, role, and regulation of mitophagy in the pressure overload model. It also pays special attention to active compounds that may regulate mitophagy in pressure overload, which provide clues for possible clinical applications.
压力超负荷导致的心脏重构和心功能障碍的病理机制尚不清楚。线粒体损伤和功能障碍，包括线粒体生物能量障碍、氧化应激和 mtDNA 损伤，导致压力超负荷引起的心脏损伤。自噬作为线粒体稳态和功能的重要调节剂，由线粒体损伤触发，并参与心血管疾病的病理过程。最近的研究表明，自噬在压力超负荷模型中起关键作用，但自噬异常与压力超负荷诱导的心脏损伤之间因果关系的证据尚不一致。本综述总结了自噬在压力超负荷模型中的机制、作用和调节，特别关注可能调节压力超负荷中自噬的活性化合物，为可能的临床应用提供线索。
