From: Regulated cell death: discovery, features and implications for neurodegenerative diseases
Type of cell death | Induction factor | Executioner | Morphological features | Biochemical halmarkers | Plasma membrane and nucleus | Chromatin | Other unique feature | Inflammatory reaction | Pharmacological inhibition |
---|---|---|---|---|---|---|---|---|---|
Apoptosis | Initiator caspases (caspase-2/8/9/10) | Executioner caspases (caspase-3/6/7) | Cellular shrinkage, dense cytoplasm, tightly packed organelles, apoptotic body formation | Activation of initiator and executioner caspases | Cell shrinkage, the plasma membrane with preserved integrity and nuclear compaction and fragmentation | Marked chromatin condensation | Apoptosome | No inflammatory reaction | Caspase-8 inhibitor, pan-caspase inhibitors |
Pyroptosis | Inflammatory caspase | GSDMD | Rupture of plasma membrane, chromatin condensation, blebbing of the cell membrane | Inflammatory caspase activation (caspase-1 and caspase-11/4/5) | Rapidly plasma-membrane rupture, cell swelling | DNA fragmentation without nuclear condensation | Inflammasome | Lytic inflammatory reaction | Inflammasome inhibitor (MCC950, Bay 1 1–7082, JC-124), pan-caspase inhibitors, caspase-1 inhibitor |
Autophagy-dependent cell death | Formation of PAS (pro-autophagosome) | Lysosomes | Focal plasma membrane rupture, autophagosome with a double-membrane, mild moderate chromatin condensation | Dependency on autophagy machinery | Focal plasma membrane rupture | Mild moderate chromatin condensation | Autophagosome | No inflammatory reaction | Autosis inhibitors |
Necroptosis | TNT, TN'FRl, FAS, TRAILR1 | MLKL | Cellular swelling, dense cytoplasm, tightly packed organelles | RIPK activation | Cell swelling; plasma membrane rupture; organelle swelling | Mild moderate chromatin condensation | Necrosomes | Inflammatory reaction | RIP1 inhibitors lnecrostaiin-1). RIP3 inhibitors (GSKS43. GSK-872).MLKL inhibitor |
Ferroptosis | Erastin, (1S, 3R)-RSL3 | Lipid peroxidation | Iron and reactive oxygen species (ROS) dependent, decreased or vanishing mitochondrial crista, a condensed mitochondrial membrane, and a ruptured outer mitochondrial membrane | Glutathione Peroxidase inactivation, iron-dependent ROS accumulation | Cell volume shrinkage and increased mitochondrial membrane density | Chromatin fragmentation | Accumulation of intracellular ROS | Inflammatory reaction | Iron chelators, (deferoxamine, DFO), lipid peroxidation inhibitors, vitamin E, ferrostatin-1 (Fer-1), and liproxstatin-1 (Lip-1) |