Targeting prostaglandin catabolism via topical nanotherapy rescues vision in ischemic optic neuropathy

levels, preserves retinal ganglion cells and optic nerve axons, and significantly improves visual function after ischemic injury. Mechanistically, 15-PGDH inhibition suppresses ferroptosis-associated lipid peroxidation and preserves mitochondrial integrity, thereby mitigating ischemia-induced neurodegeneration. Collectively, these findings establish 15-PGDH-mediated prostaglandin catabolism as a therapeutic target in ischemic optic neuropathy and demonstrate a clinically translatable nanotherapeutic strategy for protecting the central nervous system from ischemic neurodegeneration.