Ferroptosis as a double-edged sword in liver fibrosis
- VernacularTitle:铁死亡在肝纤维化中的双刃剑作用
- Author:
Yiyun AO
1
;
Anqi WU
2
;
Zhenggen WANG
3
Author Information
- Publication Type:Review
- Keywords: Hepatic Fibrosis; Ferroptosis; Hepatic Stellate Cells; Pathologic Processes
- From: Journal of Clinical Hepatology 2026;42(4):965-971
- CountryChina
- Language:Chinese
- Abstract: Ferroptosis exhibits a clear “double-edged sword” effect in liver fibrosis， with its impact strictly dependent on the type of target cells. In hepatocytes， ferroptosis induced by specific signaling pathways （such as glutathione peroxidase 4 inhibition） is a key factor for driving hepatic injury and initiating fibrogenesis， and dying hepatocytes activate hepatic stellate cells by releasing damage-associated molecules； on the contrary， in activated hepatic stellate cells， ferroptosis becomes a therapeutic target for promoting liver fibrosis regression， and selective elimination can be achieved by disrupting their distinctive antioxidant defense mechanisms. Moreover， ferroptosis modulates the dynamic balance of the fibrotic liver microenvironment by regulating macrophage polarization and intercellular communication. Based on the above mechanisms， targeting ferroptosis has emerged as a promising strategy for precise treatment. This article summarizes related research advances and discusses the major challenges and future directions for clinical translation.
