Wan Xueqi, Zhang Huan, Tian Jinfan, Hao Peng, Liu Libo, Zhou Yuquan, Zhang Jing, Song Xiantao, Ge Changjiang
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, People's Republic of China.
J Inflamm Res. 2023 Oct 16;16:4575-4592. doi: 10.2147/JIR.S430885. eCollection 2023.
Atherosclerosis (AS), a category of cardiovascular disease (CVD) that can cause other more severe disabilities, increasingly jeopardizes human health. Owing to its imperceptible and chronic symptoms, it is hard to determine the pathogenesis and precise therapeutics for AS. A novel type of programmed cell death called ferroptosis was discovered in recent years that is distinctively different from other traditional cell death pathways in morphological and biochemical aspects. Characterized by iron overload, redox disequilibrium, and accumulation of lipid hydroperoxides (L-OOH), ferroptosis influences endothelial cells, vascular smooth muscle cells (VSMCs), and macrophages, as well as inflammation, partaking in the pathology of many cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure. The mechanisms behind ferroptosis are so sophisticated and interwoven that many molecules involved in this procedure are unknown. This review systematically depicts the initiation and modulation of ferroptosis and summarizes the contribution of ferroptosis to AS, which may open a feasible approach for target treatment in the alleviation of AS progression.
动脉粥样硬化（AS）是一类可导致其他更严重残疾的心血管疾病（CVD），日益危及人类健康。由于其症状不易察觉且呈慢性，很难确定AS的发病机制和精确的治疗方法。近年来发现了一种新型的程序性细胞死亡——铁死亡，它在形态和生化方面与其他传统细胞死亡途径明显不同。铁死亡的特征是铁过载、氧化还原失衡和脂质氢过氧化物（L-OOH）积累，它影响内皮细胞、血管平滑肌细胞（VSMC）和巨噬细胞以及炎症，参与许多心血管疾病如动脉粥样硬化、中风、缺血再灌注损伤和心力衰竭的病理过程。铁死亡背后的机制非常复杂且相互交织，许多参与此过程的分子尚不清楚。本综述系统地描述了铁死亡的启动和调节，并总结了铁死亡对AS的作用，这可能为缓解AS进展的靶向治疗开辟一条可行的途径。
