Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice

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• 作者：Richard Gordan ; Nadezhda Fefelova ; Judith K. Gwathmey ; Lai-Hua Xie ; ^{xiela@njms.rutgers.edu}
• 关键词：CaWs ; Ca2+ waves ; FCCP ; carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone ; CsA ; cyclosporin A ; CypD KO ; CypD knockout mouse model ; DHPR ; α1 subunit of L-type Ca channel ; dihydropyridine receptor ; Cai2+ ; intracellular Ca2+ ; I/R ; ischemia/reperfusion ; mCU ; mitochondrial calcium uniporter ; ∆Ψ_m ; mitochondrial membrane potential ; mPTP ; mitochondrial permeability transition pore ; mNCX ; Na+-Ca2+ exchanger ; PCL ; pacing cycle length ; PLN ; phospholamban ; RyR ; ryanodine receptors ; SR ; sarcoplasmic
• 刊名：Cell Calcium
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：60
• 期：6
• 页码：363-372
• 全文大小：2474 K
• 卷排序：60

文摘

Mitochondrial Ca2+ efflux via mPTP opening increases Ca2+ wave generation. Mitochondrial Ca2+ efflux promotes Ca2+ alternans in single cells. mPTP inhibition reduces the Ca2+ wave rate and incidence of Ca2+ alternans. Ca2+ efflux via mPTP is likely involved in FCCP- and I/R-induced arrhythmias. mPTP inhibition reduces susceptibility to FCCP and I/R-induced arrhythmias.