Ferroptosis is a distinct form of regulated cell death characterised by:

• A RIPK3-MLKL-mediated plasma membrane rupture
• B Caspase-1-dependent IL-18 and IL-1β release
• C Caspase-independent lipid peroxidation requiring iron and depletion of GPX4 ✓
• D BAX-mediated cytochrome c release activating apoptosome

Explanation

Ferroptosis is a non-apoptotic, iron-dependent form of regulated cell death driven by accumulation of lipid peroxides in cell membranes. GPX4 (glutathione peroxidase 4) is the key enzyme that normally detoxifies phospholipid hydroperoxides; its inactivation allows iron-catalysed Fenton reactions to generate lethal lipid ROS. It is morphologically distinct from apoptosis (no chromatin condensation, caspase-independent) and implicated in neurodegeneration and AKI. RIPK3-MLKL defines necroptosis; caspase-1 and IL-1β/IL-18 define pyroptosis; BAX/cytochrome c defines the intrinsic apoptosis pathway.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.