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, Ca2+/CaM, P53RRA | Inducer cisplatin, erastin, DHA, STYK1 | [142, 169–174, 177, 178, 187] |