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Retinal ganglion cell (RGC) death is the critical pathological cause of irreversible visual impairment and blindness in ON injury. We previously investigated the patterns of 11 modes of cell death in mouse retina post\u2010ON injury. Here we aimed to identify additional signalling pathways regulating RGC survival in rodents post\u2010ON injury. RNA sequencing analysis identified the upregulation of inflammation and cellular senescence\u2010related genes in retina post\u2010ON injury, which were confirmed by immunoblotting and immunofluorescence analyses. Increased expression of senescence\u2010associated \u03b2\u2010galactosidase (SA\u2010\u03b2gal) in RGCs and activation of microglia were also found. Transforming growth factor\u2010\u03b2 receptor type II inhibitor (LY2109761) treatment suppressed p15<jats:sup>Ink4b<\/jats:sup> and p21<jats:sup>Cip1<\/jats:sup> protein and SA\u2010\u03b2gal expression and promoted RGC survival post\u2010ON injury with decreasing the expression of cell death markers in retina. Consistently, senolytics (dasatinib and quercetin) treatments can promote RGC survival and alleviate the reduction of ganglion cell complex thickness and pattern electroretinography activity post\u2010ON injury with reducing SA\u2010\u03b2gal, p15<jats:sup>Ink4b<\/jats:sup>, p21<jats:sup>Cip1<\/jats:sup>, microglial activation and cell death marker expression. In summary, this study revealed the activation of cellular senescence in rodent retina post\u2010ON injury and contribute to RGC survival regulation. Targeting cellular senescence can promote RGC survival after ON injury, suggesting a potential treatment strategy for traumatic optic neuropathy.<\/jats:p>","DOI":"10.1111\/cpr.13719","type":"journal-article","created":{"date-parts":[[2024,7,18]],"date-time":"2024-07-18T07:18:44Z","timestamp":1721287124000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Cellular senescence mediates retinal ganglion cell survival regulation post\u2010optic nerve crush injury"],"prefix":"10.1111","volume":"57","author":[{"given":"Yao","family":"Yao","sequence":"first","affiliation":[{"name":"Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong  Shantou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Bin","sequence":"additional","affiliation":[{"name":"Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong 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