{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T10:43:09Z","timestamp":1784976189465,"version":"3.55.0"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,5,7]]},"abstract":"\n Background<\/jats:title>\n \n Dysfunctional mitochondria are associated with neurological injury after cardiac arrest (\n CA<\/jats:styled-content>\n ). Although carbon monoxide (\n CO<\/jats:styled-content>\n ) has shown various potential therapeutic effects in preclinical tissue injury models, its mechanism of action in\n CA<\/jats:styled-content>\n remains unclear. We sought to investigate the effects of a novel\n CO<\/jats:styled-content>\n \u2010releasing molecule on cerebral mitochondrial dysfunction and neurological injury after\n CA<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n Male Sprague\u2010Dawley rats aged 20 to 22\u00a0months were subjected to 6\u2010minute asphyxia\n CA<\/jats:styled-content>\n before receiving\n CO<\/jats:styled-content>\n treatment. Survival, neurologic deficit scores, neuronal death, mitochondrial function, and autophagy were evaluated after the return of spontaneous circulation. Results showed\n that CO<\/jats:styled-content>\n post\u2010treatment increased 3\u2010day survival rate from 25% to 70.83% and reduced neurologic deficit scores.\n CO<\/jats:styled-content>\n also ameliorated\n CA<\/jats:styled-content>\n \u2010induced neuronal apoptosis and necrosis in the cerebral cortex and improved cerebral mitochondrial function by reducing reactive oxygen species, reversing mitochondrial membrane potential depolarization, and preventing cytochrome C release. Furthermore,\n CO<\/jats:styled-content>\n increased mitochondrial autophagy by inducing mitochondrial accumulation of\n PINK<\/jats:styled-content>\n 1 (\n PTEN<\/jats:styled-content>\n \u2010induced putative kinase 1) and Parkin. Downregulation of\n PINK<\/jats:styled-content>\n 1 with genetic silencing si\n RNA<\/jats:styled-content>\n abolished\n CO<\/jats:styled-content>\n \u2010afforded mitochondrial autophagy.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Taken together, our results indicate, for the first time, that\n CO<\/jats:styled-content>\n treatment confers neuroprotection against ischemic neurological injury after\n CA<\/jats:styled-content>\n possibly by promoting mitochondrial autophagy.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.118.011851","type":"journal-article","created":{"date-parts":[[2019,4,29]],"date-time":"2019-04-29T09:00:31Z","timestamp":1556528431000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":16,"title":["Novel Role of Carbon Monoxide in Improving Neurological Outcome After Cardiac Arrest in Aged Rats: Involvement of Inducing Mitochondrial Autophagy"],"prefix":"10.1161","volume":"8","author":[{"given":"Jun","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Ultrasonography Medicine The Affiliated Suzhou Hospital of Nanjing University of Chinese Medicine Suzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine The First Affiliated Hospital of Soochow University Suzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine The First Affiliated Hospital of Soochow University Suzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaping","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pathology The Affiliated Suzhou Hospital of Nanjing University of Chinese Medicine Suzhou 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