Ferroptosis is a recently characterized form of regulated cell death distinct from apoptosis and necroptosis. It is specifically driven by:
- A Activation of caspase-3 via cytochrome c release
- B MLKL phosphorylation by RIPK3 causing plasma membrane rupture
- C Gasdermin D pore formation releasing IL-1β
- D Iron-dependent lipid peroxidation of polyunsaturated fatty acid membrane phospholipids ✓
Explanation
Ferroptosis is characterized by iron-dependent accumulation of lethal lipid peroxides in cell membranes, driven by inactivation of GPX4 (glutathione peroxidase 4) which normally neutralizes lipid hydroperoxides. It does not involve caspases (apoptosis), MLKL/RIPK3 (necroptosis), or gasdermin D (pyroptosis). Ferroptosis has emerging importance in ischemia-reperfusion injury and cancer therapy resistance.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.