{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yoval-Sanchez B"],"funding":["American Heart Association","Bundesministerium für Bildung und Forschung","Deutsche Forschungsgemeinschaft","NHLBI NIH HHS","NINDS NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["102258"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8861397"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["51"],"pubmed_abstract":["Pathologies associated with tissue ischemia/reperfusion (I/R) in highly metabolizing organs such as the brain and heart are leading causes of death and disability in humans. Molecular mechanisms underlying mitochondrial dysfunction during acute injury in I/R are tissue-specific, but their details are not completely understood. A metabolic shift and accumulation of substrates of reverse electron transfer (RET) such as succinate are observed in tissue ischemia, making mitochondrial complex I of the respiratory chain (NADH:ubiquinone oxidoreductase) the most vulnerable enzyme to the following reperfusion. It has been shown that brain complex I is predisposed to losing its flavin mononucleotide (FMN) cofactor when maintained in the reduced state in conditions of RET both in vitro and in vivo. "],"journal":["Redox biology"],"pubmed_title":["Redox-dependent loss of flavin by mitochondria complex I is different in brain and heart."],"pmcid":["PMC8861397"],"funding_grant_id":["SFB815/Z1","834220","R01 NS112381","R01HL132918","R01 HL132918","R01 HL151447","R01 NS100850","R01HL151447","NS100850","RO1NS112381","S10 OD030335"],"pubmed_authors":["Sosunov S","Wittig I","Yoval-Sanchez B","Tikhonova IG","Ansari F","Filipenko P","James J","Ten V","Rafikov R","Niatsetskaya Z","Galkin A"],"additional_accession":[]},"is_claimable":false,"name":"Redox-dependent loss of flavin by mitochondria complex I is different in brain and heart.","description":"Pathologies associated with tissue ischemia/reperfusion (I/R) in highly metabolizing organs such as the brain and heart are leading causes of death and disability in humans. Molecular mechanisms underlying mitochondrial dysfunction during acute injury in I/R are tissue-specific, but their details are not completely understood. A metabolic shift and accumulation of substrates of reverse electron transfer (RET) such as succinate are observed in tissue ischemia, making mitochondrial complex I of the respiratory chain (NADH:ubiquinone oxidoreductase) the most vulnerable enzyme to the following reperfusion. It has been shown that brain complex I is predisposed to losing its flavin mononucleotide (FMN) cofactor when maintained in the reduced state in conditions of RET both in vitro and in vivo. ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2026-04-08T08:25:16.516Z","creation":"2025-02-19T03:26:18.909Z"},"accession":"S-EPMC8861397","cross_references":{"pubmed":["35189550"],"doi":["10.1016/j.redox.2022.102258"]}}