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Ubiquitin\u2010specific protease 29 (USP29) is abundantly expressed in the brain and plays critical roles in regulating oxidative stress and cell apoptosis. The purpose of the present study is to investigate the role and underlying mechanisms of USP29 in cerebral I\/R injury. Neuron\u2010specific USP29 knockout mice were generated and subjected to cerebral I\/R surgery. For USP29 overexpression, mice were stereotactically injected with the adenoassociated virus serotype 9 vectors carrying USP29 for 4 weeks before cerebral I\/R. And primary cortical neurons were isolated and exposed to oxygen glucose deprivation\/reperfusion (OGD\/R) stimulation to imitate cerebral I\/R injury in vitro. USP29 expression was elevated in the brain and primary cortical neurons upon I\/R injury. Neuron\u2010specific USP29 knockout significantly diminished, whereas USP29 overexpression aggravated cerebral I\/R\u2010induced oxidative stress, apoptosis, and neurological dysfunction in mice. In addition, OGD\/R\u2010induced oxidative stress and neuronal apoptosis were also attenuated by USP29 silence but exacerbated by USP29 overexpression in vitro. Mechanistically, neuronal USP29 enhanced p53\/miR\u201034a\u2010mediated silent information regulator 1 downregulation and then promoted the acetylation and suppression of brain and muscle ARNT\u2010like protein, thereby aggravating oxidative stress and apoptosis upon cerebral I\/R injury. Our findings for the first time identify that USP29 upregulation during cerebral I\/R may contribute to oxidative stress, neuronal apoptosis, and the progression of cerebral I\/R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I\/R injury.<\/jats:p>","DOI":"10.1155\/2021\/6955628","type":"journal-article","created":{"date-parts":[[2021,11,16]],"date-time":"2021-11-16T16:20:07Z","timestamp":1637079607000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Ubiquitin\u2010Specific Protease 29 Exacerbates Cerebral Ischemia\u2010Reperfusion Injury in 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