From Iron Metabolism to Ferroptosis: Pathologic Changes in Coronary Heart Disease

Table 1

Comparison of different forms of programmed cell death.

Cell death mode	Morphological characteristics	Biochemical features	Characteristic molecules	References
Apoptosis	Chromatin condensation, nuclear fixation, cell shrinkage, membrane blistering, and formation of apoptotic bodies	DNA fragmentation, no leakage of cell contents, no inflammatory reaction	Caspase 3, caspase 7, caspase 8, BCL-2, Bax, P53, Fas	[34, 35]
Autophagy	Accumulation of double-membraned autophagic vesicles	Increased lysosomal activity	Beclin 1, mTOR, ATG5, ATG7, LC3, TFEB, DRAM-3	[35]
Pyroptosis	Nuclear consolidation, plasma membrane pore formation, cell swelling and rupture	DNA fragmentation and inflammatory cascade response	NLRP3, ASC, pro-caspase 1, IL-1β, IL-18	[4, 36]
Ferroptosis	Mitochondrial shrinkage, increased membrane density, decreased mitochondrial cristae, and outer membrane rupture	Iron overload, lipid peroxidation, mitochondrial membrane potential changes	ACSL4, LPCAT3, xCT, GPX4, Fer-1, OxPLs, TfR1, SLC7A11, Nrf2, NCOA4	[37, 38]