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

ABSTRACT: In the present study, we have used a genetic mouse model that lacks cyclophilin D (CypD KO) to assess the cardioprotective effect of mitochondrial permeability transition pore (mPTP) inhibition on Ca²⁺ waves and Ca²⁺ alternans at the single cell level, and cardiac arrhythmias in whole-heart preparations. The protonophore carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) caused mitochondrial membrane potential depolarization to the same extent in cardiomyocytes from both WT and CypD KO mice, however, cardiomyocytes from CypD KO mice exhibited significantly less mPTP opening than cardiomyocytes from WT mice (p<0.05). Consistent with these results, FCCP caused significant increases in CaW rate in WT cardiomyocytes (p<0.05) but not in CypD KO cardiomyocytes. Fu

SUBMITTER: Gordan R 

PROVIDER: S-EPMC5127715 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature