ACSL4：急性冠脉综合征中铁死亡的关键靶点
ACSL4: Key Targets of Ferroptosis in Acute Coronary Syndrome
摘要: 急性冠脉综合征(acute coronary syndrome, ACS)具有起病急、病死率高及预后差异显著等特点，尽管再灌注治疗不断进步，其缺血再灌注损伤及远期心室重构仍缺乏有效干预靶点。铁死亡作为一种由铁依赖性脂质过氧化驱动的程序性细胞死亡方式，近年来被认为参与ACS发生发展的关键病理过程。长链酰基辅酶A合成酶4 (acyl-CoA synthetase long-chain family member 4, ACSL4)可通过促进多不饱和脂肪酸活化及膜磷脂重塑，增强脂质过氧化敏感性，从而在铁死亡调控中发挥核心作用。现有研究表明，ACSL4不仅与动脉粥样硬化斑块不稳定、心肌缺血/再灌注损伤及心室重构密切相关，而且其表达及活性受多层级分子机制调控，具有潜在的诊断和治疗价值。本文围绕ACSL4介导铁死亡的分子机制、其在ACS不同病理阶段中的作用及靶向干预策略进行综述，以期为ACS的机制研究与精准治疗提供参考。
Abstract: Acute coronary syndrome (ACS) is characterized by sudden onset, high mortality, and significant variability in prognosis. Although reperfusion therapy has substantially improved short-term outcomes, effective intervention targets for ischemia-reperfusion injury and long-term ventricular remodeling remain elusive. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as an important pathogenic mechanism in ACS. Acyl-CoA synthetase long-chain family member 4 (ACSL4) is a key enzyme involved in the activation of polyunsaturated fatty acids and their incorporation into membrane phospholipids, thereby increasing cellular susceptibility to lipid peroxidation and ferroptosis. Accumulating evidence suggests that ACSL4 participates in multiple stages of ACS progression, including atherosclerotic plaque instability, cardiomyocyte injury during ischemia-reperfusion, and subsequent ventricular remodeling. In addition, ACSL4 expression and activity are regulated by multilevel molecular mechanisms, highlighting its potential diagnostic and therapeutic value. This review focuses on the molecular mechanisms of ACSL4-mediated ferrocytosis, its role in different pathological stages of ACS, and targeted intervention strategies, with the aim of providing new insights into mechanistic research and precision treatment of ACS.
文章引用：陈宇, 李淑娟. ACSL4：急性冠脉综合征中铁死亡的关键靶点[J]. 临床医学进展, 2026, 16(6): 1753-1760. https://doi.org/10.12677/acm.2026.1662392

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