活性氧在铁死亡中的机制及其与心肌缺血灌注再损伤的联系

Mechanism of Reactive Oxygen Species in Ferroptosis and Its Association with Myocardial Ischemia-Reperfusion Injury

心肌缺血导致心肌细胞死亡及心功能损害。现阶段,再灌注疗法被视为治疗心肌缺血的关键措施之一,然而其引发的心肌损伤问题亦不容忽视。在心肌缺血灌注再损伤(MIRI)的病理生理过程中,铁死亡作为一种细胞死亡形式,与氧化应激过程紧密相连,发挥着关键作用。抑制铁死亡从而减轻心肌细胞死亡,可能成为MIRI的有效治疗策略。活性氧(ROS)是铁死亡发生和发展的关键组成部分,因此研究ROS在心肌损伤细胞中铁死亡的机制,进而开发更有效和精准的缺血再灌注治疗方法,对于降低心血管疾病的社会和经济成本具有重要意义。

Myocardial ischemia causes cardiomyocyte death and impaired cardiac function,and reperfusion is one of important treatment methods currently,but myocardial damage cannot be underestimated.During pathogenesis of myocardial ischemia-reperfusion injury(MIRI),ferroptosis is a form of cell death closely related to oxidative stress.Inhibiting ferroptosis and reducing myocardial cell death may be an effective curative strategy for MIRI.Reactive oxygen species(ROS)are crucial component in occurrence and development of ferroptosis.Therefore,exploring mechanism of ROS induced ferroptosis in myocardial injury cells and developing effective and precise ischemiareperfusion therapy methods is of great significance for reducing social and economic costs of cardiovascular diseases.