Table 3.
Potential drugs, RNA, and genes that interfere with ferroptosis and ferritinophagy to affect diabetes complications.
| Potential drugs/genes that can interfere/RNA that can interfere | Possible mechanisms | Diseases | Reference |
|---|---|---|---|
| SGLT2Is | By restoring cardiac iron homeostasis, improving mitochondrial function and antioxidant stress to resist ferroptosis | DCM | [126] |
| Rosiglitazone | By reducing the content of lipid peroxidation products and iron, and then blocking the ferroptosis of renal tubular cells | DN | [19] |
| Liraglutide | By reducing oxidative stress, lipid peroxidation and iron overload | DCI | [128] |
| Fenofibrate | By raising NRF2 to inhibit ferroptosis | DN | [130] |
| Melatonin | By activating NRF2/HO-1 signaling pathway to inhibit ferroptosis of osteoblasts | T2DOP | [131] |
| Adiponectin | by restoring CPT-1 activity to resist fatty acid oxidation/peroxide imbalance-induced ferroptosis | Placental injury in GDM | [133] |
SGLT2Is, sodium-glucose cotransporter type2 inhibitors; NRF2, nuclear factor E2-related factor2; HO-1, heme oxygenase-1; CPT-1, carnitine palmityl transferase 1; DN, diabetic nephropathy; DCM, diabetic cardiomyopathy; DCI, diabetic cognitive impairment; T2DOP, T2DM-related osteoporosis; GDM, gestational diabetes mellitus.