Compensatory transporter upregulation facilitates retinal ganglion cell survival in glaucoma after MCT2 elimination (opens in new tab)

Metabolic dysfunction contributes to glaucoma progression, including through substrate availability and the presence and concentration of substrate transporters. Observations of metabolic substrate transporter loss in glaucoma, including loss of monocarboxylate transporter-2 (MCT2), have suggested there are serious implications for metabolic dysfunction on the health and survival of retinal ganglion cells (RGCs). In this study, we investigate whether MCT2 is necessary and sufficient for RGC s...