Yang Xiaoting, Wu Hui, Liu Di, Zhou Gang, Zhang Dong, Yang Qingzhuo, Liu Yanfang, Li Yi
Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Hubei Key Laboratory of Ischemic Cardiovascular Disease, Yichang, China.
J Cardiovasc Transl Res. 2025 Apr;18(2):408-423. doi: 10.1007/s12265-025-10590-6. Epub 2025 Jan 30.
Myocardial ischemia/reperfusion (I/R)-induced cell death, such as autophagy and ferroptosis, is a major contributor to cardiac injury. Regulating cell death may be key to mitigating myocardial ischemia/reperfusion injury (MI/RI). Autophagy is a crucial physiological process involving cellular self-digestion and compensation, responsible for degrading excess or malfunctioning long-lived proteins and organelles. During MI/RI, autophagy plays both "survival" and "death" roles. A growing body of research indicates that ferroptosis is a type of autophagy-dependent cell death. This article provides a comprehensive review of the functions of autophagy and ferroptosis in MI/RI, as well as the molecules mediating their interaction. Understanding the link between autophagy and ferroptosis may offer new therapeutic directions for MI/RI, bearing significant clinical implications.
心肌缺血/再灌注（I/R）诱导的细胞死亡，如自噬和铁死亡，是心脏损伤的主要原因。调节细胞死亡可能是减轻心肌缺血/再灌注损伤（MI/RI）的关键。自噬是一个关键的生理过程，涉及细胞自我消化和补偿，负责降解多余或功能失调的长寿蛋白质和细胞器。在MI/RI期间，自噬发挥着“生存”和“死亡”的作用。越来越多的研究表明，铁死亡是一种自噬依赖性细胞死亡。本文全面综述了自噬和铁死亡在MI/RI中的作用，以及介导它们相互作用的分子。了解自噬和铁死亡之间的联系可能为MI/RI提供新的治疗方向，具有重要的临床意义。
