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In this study, the middle cerebral artery occlusion\/reperfusion (MCAO\/R)-induced ischemic stroke mouse model and oxygen-glucose deprivation\/reoxygenation (OGD\/R)-treated primary neurons were used to explore the molecular mechanism of Activin A-mediated neuroprotection against ischemic injuries. We found that Activin A significantly inhibits cGAS-STING-mediated excessive autophagy through the PI3K-PKB pathway, but not mTOR-dependent autophagy. Consequently, Activin A protected neurons against OGD\/R-induced ischemic injury and improved cell survival in a dose-dependent manner. In addition, Activin A improved neurological functions and reduced infarct size of mice with MCAO\/R-induced ischemic stroke by inhibiting autophagy. Furthermore, Activin A depended on ACVR1C receptor to exert neuroprotective effects in 1\u2009h MCAO\/R treated mice. Our findings showed that Activin A alleviated neuronal ischemic injury through inhibiting cGAS-STING-mediated excessive autophagy in mice with ischemic stroke, which may suggest a potential therapeutic target for ischemic stroke.<\/jats:p>","DOI":"10.1177\/0271678x221147056","type":"journal-article","created":{"date-parts":[[2022,12,20]],"date-time":"2022-12-20T02:38:27Z","timestamp":1671503907000},"page":"736-748","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":41,"title":["Activin A alleviates neuronal injury through inhibiting cGAS-STING-mediated autophagy in mice with ischemic stroke"],"prefix":"10.1177","volume":"43","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1025-7646","authenticated-orcid":false,"given":"Meilian","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Neurobiology, School of Basic Medical Science, Capital Medical University, Beijing, PR 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