<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Technology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.2026070015</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>FDX1/ACSL4 轴调控脂过氧化与心梗铜死亡机制进展</title><url>https://artdesignp.com/journal/MRP/4/7/10.61369/MRP.2026070015</url><author>肖平,黄玲</author><pub-date pub-type="publication-year"><year>2026</year></pub-date><volume>4</volume><issue>7</issue><history><date date-type="pub"><published-time>2026-07-20</published-time></date></history><abstract>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。</abstract><keywords>急性心肌梗死,铜死亡,FDX1,ACSL4,脂质过氧化,铁死亡</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1]Welt, F. G. P. et al. Reperfusion injury in patients with acute myocardial infarction: JACC scientific statement. Journal of the American College of Cardiology 83, 2196&amp;ndash;2213 (2024).[2]Chen, X. et al. Copper homeostasis and copper-induced cell death in the pathogenesis of cardiovascular disease and therapeutic strategies. Cell Death &amp;amp; Disease 14, 105 (2023).[3]Xue, Q. et al. Copper metabolism in cell death and autophagy. Autophagy 19, 2175&amp;ndash;2195 (2023).[4]iChen, G. et al. Phillygenin ameliorates myocardial ischemia-reperfusion injury by inhibiting cuproptosis via the autophagy-lysosome degradation of CTR1. Free Radical Biology &amp;amp; Medicine 237, 542&amp;ndash;557 (2025).[5]Liu, F. et al. Janus hydrogels delivering low-density lipoprotein receptor-related protein 6 inhibitor enhance myocardial repair via m6A-dependent cuproptosis in bama pigs. Acta Biomaterialia 201, 255&amp;ndash;265 (2025).</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
