Targeting Ferroptosis for Lung Diseases: Exploring Novel Strategies in Ferroptosis-Associated Mechanisms

Table 1

Comparison of characteristics of ferroptosis and necrosis, apoptosis, autophagy, necroptosis, and pyroptosis.

Cell death manner	Morphologic features	Biochemical characteristics	Key controlling genes	References
Ferroptosis	Membrane rupture or blistering, mitochondrial atrophy, crista reduction, lack of chromatin condensation	Lipid peroxidation in cells induced by ferrous or esterase	GPX4, p53, Ras, Nox, SLC7A11, TFR1	[3, 4, 52]
Necrosis	Lipid peroxidation in cells induced by ferrous or esterase	Inflammatory response	—
Apoptosis	Cell membrane foaming, cell contraction, the formation of apoptotic bodies	DNA degradation	Bcl-2 family, caspase family, C-myc, p53	[55, 56]
Autophagy	Cytoplasmic vacuolization to form autophagosomes	Increase activity of lysosomes	ATG5, ATG7, Beclin1	[59, 199]
Necroptosis	Cell volume enlargement, organelle swelling, cell membrane perforation, with necrotic cell characteristics	Cell collapse, release contents, triggering an immune response, and clearing the dead cells through macropinocytosis bodies	RIPK1, RIPK3, TNFR1, caspase-8	[66, 67]
Pyroptosis	Cell swelling, with a large number of bubble-like protrusions; a large number of vesicles, pyroptosis bodies, formed before the rupture of the plasma membrane	Formation of inflammatory bodies, activation of caspase and gasdermin, the release of a large number of proinflammatory factors	Caspase family, NLRP3, ASC	[71–73]