Abstract
Glaucoma, a progressive age‐related optic neuropathy characterized by retinal ganglion cell degeneration and alteration of the optic nerve head, is a leading cause of irreversible blindness worldwide. Elevated intraocular pressure (IOP) is one of the main and the only known modifiable risk factor. However, despite lowering IOP, glaucomatous damage still progresses in a relevant percentage of patients.Neuroprotection in glaucoma refers to any non‐IOP related treatments that can prevent or delay neurodegeneration. Metformin (1,1‐dimethylbiguanide hydrochloride) is one of the first‐line anti‐hyperglycemic drugs for type 2 diabetes mellitus. In recent years, several studies have investigated the neuroprotective effect of metformin in a variety of neurodegenerative diseases, revealing that this drug is able to regulate energy metabolism, prevent oxidative stress, reduce neuroinflammation and trigger autophagy.The autophagy‐lysosome system, which is responsible for breaking down cellular components, preserving cellular homeostasis and preventing accumulation of protein aggregates and damaged organelles, is often dysregulated in neurodegenerative pathologies.Here we show that the neurodegeneration observed in experimental models of glaucoma is associated with autophagy and mitophagy dysregulation, and describe the neuroprotective effects of treatment with metformin as autophagy modulator. To explore the possibility of the clinical translation of our findings, we performed a retrospective pilot study documenting for the first time a putative neuroprotective effect of metformin in glaucomatous diabetic patients.
Published Version
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