Wu Xinyu, Li Jingru, Cheng Huan, Wang Luqiao
Department of Cardiology, The First Affiliated Hospital of Kunming Medical University, 650032 Kunming, Yunnan, China.
Rev Cardiovasc Med. 2024 Apr 30;25(5):149. doi: 10.31083/j.rcm2505149. eCollection 2024 May.
Acute myocardial infarction (AMI) is triggered by the blockage of coronary arteries, leading to restricted blood flow to the myocardium, which results in damage and cell death. While the traditional understanding of cell death primarily revolves around apoptosis, a new player in the game has emerged: ferroptosis. This novel form of cell death relies on iron and is propelled by reactive oxygen species (ROS). Lipid metabolism, an indispensable physiological process, plays a vital role in preserving cellular homeostasis. However, when this metabolic pathway is disrupted, the accumulation of excess waste increases, specifically lipid peroxides, which are strongly linked to the occurrence and progression of AMI. As a result, comprehending this complex interaction between ferroptosis and lipid metabolism could pave the way for new therapeutic approaches in tackling AMI.
急性心肌梗死(AMI)是由冠状动脉阻塞引发的,导致心肌血流受限,进而造成损伤和细胞死亡。虽然传统上对细胞死亡的理解主要围绕细胞凋亡,但一种新的因素出现了:铁死亡。这种新型细胞死亡形式依赖铁,并由活性氧(ROS)驱动。脂质代谢是一个不可或缺的生理过程,在维持细胞内稳态方面发挥着至关重要的作用。然而,当这条代谢途径被破坏时,过量废物的积累就会增加,特别是脂质过氧化物,它们与AMI的发生和发展密切相关。因此,理解铁死亡与脂质代谢之间这种复杂的相互作用,可能为攻克AMI的新治疗方法铺平道路。