Ferroptosis in alcoholic liver fibrosis： Mechanism of action and therapeutic strategies
- VernacularTitle:铁死亡在酒精性肝纤维化中的作用机制及其相关治疗策略
- Author:
Zhiyuan WEI
1
;
Feng LIN
1
;
Tao WU
1
Author Information
- Publication Type:Review
- Keywords: Liver Diseases， Alcoholic; Hepatic Fibrosis; Ferroptosis; Lipid Peroxides
- From: Journal of Clinical Hepatology 2026;42(5):1172-1177
- CountryChina
- Language:Chinese
- Abstract: Alcoholic liver fibrosis is a critical step in the progression of alcoholic liver disease toward liver cirrhosis， yet there is currently still a lack of effective and specific anti-fibrotic therapeutic strategies. Recent studies have shown that as an iron-dependent， lipid peroxidation-driven form of regulated cell death， ferroptosis plays an important role in alcohol-related hepatocellular injury and fibrogenesis. Reactive oxygen species generated during alcohol metabolism can damage hepatocytes， impair their antioxidant defense ability， and lead to disruption of iron homeostasis and accumulation of lipid peroxides， ultimately triggering ferroptosis. Hepatocyte ferroptosis can promote fibrosis by amplifying inflammatory responses and activating hepatic stellate cells， whereas selective induction of ferroptosis in activated hepatic stellate cells may attenuate fibrosis， highlighting the “double-edged sword” effect of ferroptosis. Current interventions against ferroptosis mainly focus on applying antioxidant approaches， reducing iron burden， or blocking the amplification of lipid peroxidation， which have shown preliminary efficacy and a potential clinical value， but there are still limitations such as single-target actions and insufficient cell selectivity. In the future， nanotechnology-based delivery and other targeting strategies may help to realize multi-pathway coordination and cell-specific modulation， thereby improving the anti-fibrotic efficacy of ferroptosis-oriented therapies.
