Ferroptosis is a recently characterized form of regulated cell death distinct from apoptosis and necroptosis. It is defined by:

• A Caspase-3 activation leading to DNA fragmentation and apoptotic body formation
• B MLKL phosphorylation causing plasma membrane rupture in necroptosis
• C Iron-dependent accumulation of lipid peroxides causing membrane damage ✓
• D Pyruvate kinase M2 dimerization causing metabolic cell death

Explanation

Ferroptosis is a form of regulated, non-apoptotic cell death driven by iron-dependent accumulation of lipid reactive oxygen species (lipid peroxidation), particularly of polyunsaturated fatty acids in membranes. GPX4 (glutathione peroxidase 4) normally detoxifies lipid peroxides; its inhibition (or GSH depletion) triggers ferroptosis. It is distinct from apoptosis (no caspases), necroptosis (no MLKL), and pyroptosis (no gasdermin). It is implicated in ischemia-reperfusion, neurodegeneration, and cancer.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.