Retinal pigment epithelium cells accumulate oxidative damage from lifetime light exposure, driving senescent phenotypes by age 60–70. Senescent RPE cells produce VEGF (driving choroidal neovascularization in wet AMD), reduce photoreceptor nutrient support, and accumulate drusen-forming lipofuscin. Senolytic clearance of aged RPE cells is an active area of research.

No confirmed human evidence exists for AMD prevention by senolytics. The mechanistic rationale (RPE senescence drives AMD) is strong, and preclinical data is promising. AMD prevention trials with senolytics are a logical next step but have not been completed.

Do senolytics lower intraocular pressure in glaucoma?

No direct human evidence. Animal models show trabecular meshwork function improvement post-senolytic treatment. Human glaucoma patients considering senolytics should maintain standard treatments.