Phosphatidylcholine modulates trabecular meshwork resilience to glaucomatous injury via regulation of TGFBR3 signaling

This integrative study demonstrated that PC(18:2/20:4) is a causal and relevant lipid modulator in pathogenesis of glaucoma. PC(18:2/20:4) protects HTMCs from pressure-induced oxidative stress, fibrosis, and apoptosis by activating the TGFBR3-AMPK/mTOR pathway. Our findings provide experimental basis for further development of lipid-based therapy to preserve HTMCs in glaucoma.