ArticleFrontiers in cell and developmental biology2026
Compensatory transporter upregulation facilitates retinal ganglion cell survival in glaucoma after MCT2 elimination.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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 survival
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