Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Ferroptosis Pathway
Ferroptosis assay is an experimental method used to assess cell death due to iron stress. In the presence of high concentrations of iron ions, excessive free radicals can be generated within cells, leading to oxidative stress and cell damage. Detection methods include fluorescent probe labeling, cell morphology observation, DNA fragmentation, etc. Ferroptosis detection is helpful in studying the relationship between cellular iron metabolism disorders and diseases, such as anemia, neurological diseases, etc. This research is of great significance for revealing the mechanism of iron action in organisms and potential therapeutic targets.
Related Experimental Schemes
