Torin 2 Restores Autophagy to Preserve Retinal Ganglion Cells in Two Glaucoma Models

The University of Missouri study used pharmacological activation of autophagy via Torin 2 in established glaucoma models. Researchers measured retinal ganglion cell survival, mitochondrial morphology, and visual function after inducing autophagy enhancement. Treated eyes retained more ganglion cells and showed improved electrophysiological responses compared with vehicle controls, linking restored mitophagy to reduced cellular stress.

Current glaucoma care centers on intraocular pressure reduction, yet many patients progress despite lowered pressure. This work highlights mitochondrial quality control failure as an independent driver of neurodegeneration. Observational human data already associate autophagic markers with optic nerve head damage, suggesting the pathway is clinically relevant beyond animal models.

Torin 2 itself is not approved for human use. The authors therefore call for selective, translatable autophagy modulators that could be combined with pressure-lowering drops. Next steps include screening approved compounds for mitophagy activity and testing them in larger animal species before any clinical trial design.

Evidence quality note: The findings derive from interventional animal experiments; they demonstrate mechanistic plausibility but cannot yet establish efficacy or safety in humans. A phase I safety study of a candidate autophagy modulator in glaucoma patients is required next.