| Popis: |
Ferroptosis is a form of cell death that results from accumulation of lipid reactive oxygen species, marked by iron-dependent oxidative damage of phospholipids. Accumulation of iron and lipid hydroperoxides are hallmarks of ferroptosis. Diverse biological contexts, including iron handling, redox homeostasis, imbalance of lipid synthesis, participate in ferroptosis. Mechanistically, pathways of ferroptosis regulation involving System Xc--glutathione (GSH)-glutathione peroxidase 4 (GPX4) axis, coenzyme Q10 (CoQ10)-ferroptosis suppressor protein 1 (FSP1)-ubiquinol axis, GTP cyclohydrolase 1 (GCH1)-tetrahydrobiopterin (BH4)-dihydrofolate reductase (DHFR) axis, dehydrogenase (DHODH)-ubiquinol axis have been discovered. Ferroptosis has been implicated in multiple liver diseases, such as hepatocellular carcinoma, liver ischemia-reperfusion injury, steatohepatitis, liver fibrosis, cirrhosis and liver metabolic diseases. Elucidating its mechanism offers various tractable nodes for therapeutic intervention. Here, we summarize insights into the molecular characteristics, biological processes, regulatory pathways of ferroptosis and its recent advances in the treatment of liver diseases. |
