Targeting ferroptosis in metabolic dysfunction‑associated steatotic liver disease: From mechanisms to cell type‑specific therapeutic strategies (Review).

Metabolic dysfunction‑associated steatotic liver disease (MASLD) impacts >30% of the global population. Its progression to metabolic dysfunction‑associated steatohepatitis and liver fibrosis is the primary determinant for cirrhosis and hepatocellular carcinoma. Ferroptosis depends on iron and is driven by lipid peroxidation and is involved in the development of MASLD. Effective anti‑fibrotic agents remain an unmet clinical need. The present review aimed to summarize the metabolic environment in MASLD, which is characterized by lipid overload, iron dysregulation and oxidative stress, and its role in facilitating ferroptosis using a cell type‑ and disease stage‑specific framework, integrating intercellular crosstalk and evidence grading for biomarkers and therapeutic agents, as well as knowledge gaps, such as the paucity of direct human evidence, unresolved spatiotemporal dynamics and the necessity for precision delivery systems. The present review positions ferroptosis as a key pathophysiological element in MASLD and a promising frontier for diagnostic and therapeutic innovation by combining mechanistic insight with translational perspectives.