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

Table 2

The role and mechanism of ferroptosis in pulmonary diseases.

Disease	Research object	Biochemical features	Regulation mechanism	Inhibitors/inducers	References
COVID-19	Serum	Thrombosis, accumulation of oxidized phospholipids	Hepcidin	—	[124, 125, 130]
ALI	Human bronchial epithelial cells BEAS-2B and mouse lung cells	Lung inflammation out of control, oxidation/antioxidant imbalance	Nrf2/HIF-1, Nrf2/HO-1/SLC7A11, p62/Keap1/Nrf2 axis, PTGS2	Inhibitor Fer-1	[102, 133, 135, 137, 145]
PF	Human fetal lung fibroblasts HFL1, RILF mouse lung tissue cells	Increased ROS, lipid peroxidation, and fibroblast differentiation	α-SMA, COLI, Nrf2/HO-1/NQO1	Inhibitor Fer-1, Lip-1	[87, 151]
COPD	Human bronchial epithelial cells and mouse mode	Lipid peroxidation increased production of 4-HNE and DAMPs	NCOA4, GPX4	Inhibitor, deferoxamine, and Fer-1	[154, 155]
Lung cancer	NSCLC cell SW900, human plasma	Upregulation of GPX4/GSH pathway, reduction of iron, inhibition of lipid synthesis, and upregulation of FSP1	NF2-YAP, ACSL4, PRIM2/SLC7A11 axis, Nrf2/HO-1 axis, Ca^2+/CaM, P53RRA	Inducer cisplatin, erastin, DHA, STYK1	[142, 169–174, 177, 178, 187]