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This study is to determine the role of Akt S\u2010Nitrosylation in the recovery of heart functions after ischaemia. In recombinant Akt protein and in HEK293 cells, NO donor decreased Akt activity and induced Akt S\u2010Nitrosylation, but was abolished if Akt protein was mutated by replacing cysteine 296\/344 with alanine (Akt\u2010C296\/344A). In endothelial cells, NO induced Akt S\u2010Nitrosylation, reduced Akt activity and damaged multiple cellular functions including proliferation, migration and tube formation. These alterations were ablated if cells expressed Akt\u2010C296\/344A mutant. In <jats:italic>Apoe<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice, nitroglycerine infusion increased both Akt S\u2010Nitrosylation and infarct size, reduced Akt activity and capillary density, and delayed the recovery of cardiac function in ischaemic hearts, compared with mice infused with vehicle. Importantly, these in vivo effects of nitroglycerine in <jats:italic>Apoe<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice were remarkably prevented by adenovirus\u2010mediated enforced expression of Akt\u2010C296\/344A mutant. In conclusion, long\u2010term usage of organic nitrate may inactivate Akt to delay ischaemia\u2010induced revascularization and the recovery of cardiac function through NO\u2010mediated S\u2010Nitrosylation.<\/jats:p>","DOI":"10.1111\/jcmm.15263","type":"journal-article","created":{"date-parts":[[2020,10,31]],"date-time":"2020-10-31T02:53:45Z","timestamp":1604112825000},"page":"27-36","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["S\u2010Nitrosylation of Akt by organic nitrate delays revascularization and the recovery of cardiac function in mice following myocardial infarction"],"prefix":"10.1111","volume":"25","author":[{"given":"Xiao\u2010Yan","family":"Li","sequence":"first","affiliation":[{"name":"Department of Cardiology the 960<sup>th<\/sup>Hospital of Chinese People's Liberation Army Jinan 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