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Table 1 Comparison of different types of cell death

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)