Volume 4,Issue 7
FDX1/ACSL4 轴调控脂过氧化与心梗铜死亡机制进展
急性心肌梗死（AMI）后持续性的心肌细胞死亡是导致心功能恶化和不良重构的关键环节。近年来，铜死亡作为一种由铜离子稳态失衡触发、依赖线粒体代谢的新型调节性细胞死亡方式，在AMI中的作用受到广泛关注。现有研究提示，由FDX1（铁氧还蛋白1）和ACSL4（长链脂酰辅酶A合成酶4）构成的功能轴，可能通过耦联铜还原反应、活性氧生成和脂质过氧化放大，驱动AMI中心肌细胞铜死亡。本文围绕FDX1/ACSL4轴的分子功能、介导脂质过氧化的关键机制、与铁死亡等通路的关系及其靶向干预前景进行综述，以期为AMI精准心肌保护提供新的理论依据。与单纯从氧化应激或炎症反应解释AMI损伤不同，该轴更强调金属离子失衡、线粒体毒性和膜脂破坏之间的连续病理链条。
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