Drug | Mechanism | Role | Diseases | Physiologic effects | References |
---|---|---|---|---|---|
Chloroquine (CQ) & hydroxychloroquine (HCQ) | Autophagy inhibition to Autophagosome & Lysosome | Harmful | Glaucoma | Treatment of CQ and HCQ causes RGC and retinal damage | |
Diabetic retinopathy | CQ worsens the progression of diabetic retinopathy | [248] | |||
Blindness | Rheumatic patients treated with HCQ leads to blindness | [247] | |||
Rapamycin | Autophagy activation by mTORC1 inhibition | Protective | Glaucoma | Rapamycin is neuroprotective in a chronic hypertensive glaucoma model and increases RGC survival following optic nerve transection | |
AMD | Rapamycin prevents AMD-related aging of RPE cells | [222] | |||
Diabetic retinopathy | Rapamycin ameliorates the high glucose-induced ROC in the RPE | [223] | |||
Optic neuropathy | Rapamycin-induced autophagy results in less damage from G11778A mutation, the most common cause of Leber’s hereditary optic neuropathy | [225] | |||
Everolimus | Autophagy activation by mTORC1 inhibition | Protective | Glaucoma | Everolimus suppresses the scar formation in glaucoma filtering surgery in an animal model | [226] |
AMD | Everolimus suppresses angiogenesis molecular pathways in the onset of wet AMD | [228] | |||
Diabetic retinopathy | Everolimus suppresses angiogenesis molecular pathways in the onset of diabetic retinopathy | [229] | |||
Harmful | Optic neuropathy | Long-term administration of everolimus may cause reversible encephalopathy syndrome and bilateral optic neuropathy after kidney transplantation | |||
Temsirolimus | Autophagy activation by mTORC1 inhibition | Protective | AMD | Temsirolimus inhibits RPE and endothelial cell proliferation and decreases VEGF and PDGF expression | [233] |
Diabetic retinopathy | Temsirolimus is considered as an antiangiogenic drug for diabetic retinopathy progression | [234] | |||
Metformin | Autophagy activation by AMPK activation and subsequent inhibition of mTORC1 signaling | Protective | Glaucoma | Metformin is used to control blood sugar and is considered to reduce the risk of the onset of glaucoma, AMD, and diabetic retinopathy in diabetic patients | |
AMD | |||||
Diabetic retinopathy | |||||
Lithium (LiCl) | Autophagy activation by mTOR-independent pathway | Protective | Glaucoma | In animal studies, LiCl was reported as an autophagy inducer, which could alleviate the progression of glaucoma, diabetic retinopathy, and optic neuropathy | |
Diabetic retinopathy | |||||
Optic neuropathy | |||||
Ripasudil | Autophagy activation by inhibition of rho-associated coiled-coil containing protein kinase 1 (ROCK1) | Protective | Glaucoma | Ripasudil is the key component in ophthalmic solutions for treating glaucoma by reducing IOP Ripasudil promotes axonal protection in an animal model | |
Steroids | Autophagy activation by GABAA receptor | Protective | Retinal degeneration | Neurosteroids induces the autophagy pathway to protect retinal neurons | [218] |
Inhibiting autophagosome biogenesis pathway | Harmful | Glaucoma | Steroid therapy in the eye leads to the dysregulation of TMCs and develop glaucoma pathology | [219] |