Cui Shaojie, Ye Jin
College of Biomedicine and Health, College of Life Science and Technology, Huazhong Agricultural University, Wuhan, Hubei 430070, China.
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Trends Mol Med. 2025 Sep 9. doi: 10.1016/j.molmed.2025.08.006.
Ferroptosis, a regulated cell death pathway driven by iron-catalyzed lipid peroxidation, has recently been implicated as a major cause of hepatic injury in metabolic dysfunction-associated fatty liver disease (MAFLD). This review highlights how the identification of hyperoxidized peroxiredoxin 3 (PRDX3) as a ferroptosis-specific marker has led to the discovery that ferroptosis contributes to liver injury in MAFLD, and summarizes other emerging evidence connecting ferroptosis to MAFLD pathogenesis. These new findings suggest that dietary fat composition and genetic variants such as PNPLA3(I148M) may affect the progression of MAFLD by regulating cellular sensitivity to ferroptosis. Recognizing MAFLD as a ferroptotic disease provides novel insights into the pathogenesis of the disease, and supports the exploration of ferroptosis as a potential target for therapeutic intervention.
铁死亡是一种由铁催化的脂质过氧化驱动的程序性细胞死亡途径,最近被认为是代谢功能障碍相关脂肪性肝病(MAFLD)肝损伤的主要原因。本综述强调了高氧化的过氧化物酶体增殖物激活受体3(PRDX3)作为铁死亡特异性标志物的鉴定如何促使人们发现铁死亡在MAFLD肝损伤中起作用,并总结了将铁死亡与MAFLD发病机制联系起来的其他新证据。这些新发现表明,饮食脂肪成分和PNPLA3(I148M)等基因变异可能通过调节细胞对铁死亡的敏感性来影响MAFLD的进展。将MAFLD视为一种铁死亡性疾病为该疾病的发病机制提供了新的见解,并支持将铁死亡作为治疗干预的潜在靶点进行探索。