Matches in SemOpenAlex for { <https://semopenalex.org/work/W4225972051> ?p ?o ?g. }
- W4225972051 abstract "Glaucoma is a leading cause of irreversible blindness worldwide and is characterized by progressive optic nerve degeneration and retinal ganglion cell loss. Axonal transport deficits have been demonstrated to be the earliest crucial pathophysiological changes underlying axonal degeneration in glaucoma. Here, we explored the role of the tetraspanin superfamily member CD82 in an acute ocular hypertension model. We found a transient downregulation of CD82 after acute IOP elevation, with parallel emergence of axonal transport deficits. The overexpression of CD82 with an AAV2/9 vector in the mouse retina improved optic nerve axonal transport and ameliorated subsequent axon degeneration. Moreover, the CD82 overexpression stimulated optic nerve regeneration and restored vision in a mouse optic nerve crush model. CD82 exerted a protective effect through the upregulation of TRAF2, which is an E3 ubiquitin ligase, and activated mTORC1 through K63-linked ubiquitylation and intracellular repositioning of Raptor. Therefore, our study offers deeper insight into the tetraspanin superfamily and demonstrates a potential neuroprotective strategy in glaucoma treatment." @default.
- W4225972051 created "2022-05-05" @default.
- W4225972051 creator A5003388740 @default.
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- W4225972051 creator A5079906197 @default.
- W4225972051 date "2021-12-11" @default.
- W4225972051 modified "2023-10-16" @default.
- W4225972051 title "CD82 protects against glaucomatous axonal transport deficits via mTORC1 activation in mice" @default.
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- W4225972051 doi "https://doi.org/10.1038/s41419-021-04445-6" @default.
- W4225972051 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34897284" @default.