Glaucoma, a progressive age-related optic neuropathy characterized by retinal ganglion cell degeneration and alteration of the optic nerve head is a worldwide leading cause of irreversible blindness. Elevated intraocular pressure (IOP), is one of the main, and the only modifiable, risk factor. However, despite the efficient control of IOP values (either pharmacologically or surgically), the loss of retinal ganglion cells progresses in a significant percentage of patients suggesting that IOP-independent, and still unidentified factors, are relevant for the onset and evolution of the disease.
Dysregulation of the autophagy-lysosome system, which is responsible responsible for the selective e non-selectivedegradation of proteins and organelles, has been associated with several central and peripheral neurodegenerative pathologies although its role in glaucoma-related neurodegeneration is still debated.
Here we show that neurodegeneration observed in experimental models of glaucoma is associated with autophagy and mitophagy dysregulation, and explore the pharmacological modulation of the process as potential neuroprotective strategy.

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