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10.1038/s44161-025-00752-9 http://scihub22266oqcxt.onion/10.1038/s44161-025-00752-9 41381906!?!41381906 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41381906&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Nat+Cardiovasc+Res 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41381906|t=2025. Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia |pdf=|usr=}}{{41381906}} gab.com Text Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia JO: Nat Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=41381906 #FOAvip The mitochondrial membrane potential (DeltaPsi(m)) drives oxidative phosphorylation and alterations contribute to cardiac pathologies, but real-time assessment of DeltaPsi(m) has not been possible. Here we describe noninvasive measurements using mitochondrial heme b(L) and b(H) absorbances, which rapidly respond to DeltaPsi(m). Multi-wavelength absorbance spectroscopy enabled their continuous monitoring in isolated mitochondria and the perfused heart. Calibration of heme b absorbance in isolated mitochondria revealed that reduced heme b(L) relative to total reduced heme b (fb(L) = b(L)/(b(L) + b(H))) exhibits a sigmoidal relationship with DeltaPsi(m). Extrapolating this relationship to the heart enabled estimation of DeltaPsi(m) as 166 +/- 18 mV (n = 25, mean +/- s.d.). We used this approach to assess how DeltaPsi(m) changes during ischemia-reperfusion injury, an unknown limiting the understanding of ischemia-reperfusion injury. In perfused hearts, DeltaPsi(m) declined during ischemia and rapidly reestablished upon reperfusion, supported by oxidation of the succinate accumulated during ischemia. These findings expand our understanding of ischemia-reperfusion injury. Twit Text FOAVip Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia ????Nat Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=41381906 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41381906 #FOAvip English Wikipedia <ref>{{Cite pmid|41381906}}</ref> Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia #MMPMID41381906 Giles AV; Covian R; Prag HA; Burger N; Lucotte B; Yu CS; Sun J; Murphy E; Krieg T; Murphy MP; Balaban RS Nat Cardiovasc Res 2025[Dec]; ? (?): ? PMID41381906show ga The mitochondrial membrane potential (DeltaPsi(m)) drives oxidative phosphorylation and alterations contribute to cardiac pathologies, but real-time assessment of DeltaPsi(m) has not been possible. Here we describe noninvasive measurements using mitochondrial heme b(L) and b(H) absorbances, which rapidly respond to DeltaPsi(m). Multi-wavelength absorbance spectroscopy enabled their continuous monitoring in isolated mitochondria and the perfused heart. Calibration of heme b absorbance in isolated mitochondria revealed that reduced heme b(L) relative to total reduced heme b (fb(L) = b(L)/(b(L) + b(H))) exhibits a sigmoidal relationship with DeltaPsi(m). Extrapolating this relationship to the heart enabled estimation of DeltaPsi(m) as 166 +/- 18 mV (n = 25, mean +/- s.d.). We used this approach to assess how DeltaPsi(m) changes during ischemia-reperfusion injury, an unknown limiting the understanding of ischemia-reperfusion injury. In perfused hearts, DeltaPsi(m) declined during ischemia and rapidly reestablished upon reperfusion, supported by oxidation of the succinate accumulated during ischemia. These findings expand our understanding of ischemia-reperfusion injury. ?Rapid mitochondrial repolarization upon reperfusion after cardiac isch(epmc).pdf DeepDyve Pubget Overpricing