ArticleDiagnostic pathology2025
SHMT2 overexpression improves glaucoma by enhancing mitophagy in retinal ganglion cells through promoting the phospho of PINK1.
Article in Diagnostic pathology, 2025. 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
backgroundGlaucoma is a major eye disease that causes blindness. The loss of retinal ganglion cells (RGCs) due to mitophagy impairment is a key driver of glaucoma. SHMT2 depletion leads to an increase in reactive oxygen species (ROS), but its role in regulating mitophagy remains unclear. This study aims to investigate the mechanism by which SHMT2 contributes to glaucoma through the regulation of RGC mitophagy.
methodsThe role of SHMT2 in glaucoma was evaluated through hematoxylin and eosin (H&E) staining and immunofluorescence (IF) staining of acute ocular hypertension (AOH) mouse eyeballs. Mitophagy was assessed by measuring LDH release, apoptosis, mitochondrial membrane potential, lipid ROS, and the protein levels of mitophagy-related proteins in RGCs. The underlying mechanism was investigated using co-immunoprecipitation, IF staining, and Western blot analysis.
resultsResults showed that SHMT2 expression was decreased in the AOH mouse model. NMDA inhibited mitophagy in RGCs, which was restored by SHMT2 overexpression. Moreover, SHMT2 overexpression stabilized PINK1 expression by enhancing the phosphorylation of PINK1. In vivo experiments suggested that SHMT2 overexpression increased the thickness of the retinal ganglion cell-inner plexiform layer.
conclusionThis study confirmed that SHMT2 overexpression alleviated glaucoma by enhancing mitophagy in RGCs through the upregulation of PINK1 phosphorylation, suggesting that SHMT2 may serve as a potential therapeutic target for glaucoma.
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