The findings from a recent eLife study were featured in a Q&A in The Ophthalmologist, highlighting Duke Eye Center research led by Simon John, PhD, Dan Stamer, PhD, Jiang Qian, PhD, Nicholas Tolman, and Taibo Li. Their work used single‑cell epigenomic profiling to uncover previously unrecognized diversity within the trabecular meshwork (TM), identifying a metabolically vulnerable TM cell subtype whose mitochondrial dysfunction contributes to elevated intraocular pressure in a glaucoma mouse model. Importantly, the team demonstrated that vitamin B3 (nicotinamide) can protect these cells, prevent pressure elevation, and reduce glaucoma development by supporting mitochondrial health.
This research opens the door to a new therapeutic strategy focused on strengthening cellular metabolism—an approach distinct from current pressure‑lowering treatments. Because nicotinamide has shown protective effects in both TM cells and retinal ganglion cells, it represents a promising candidate for future prophylactic or adjunctive glaucoma therapies. Ongoing work aims to determine whether similar TM cell subtypes exist in humans and to advance metabolism‑targeted treatments into clinical studies.