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- W2002907780 abstract "The mechanism through which metformin confers cardioprotection in clinical studies is unknown. Studies suggest that metformin can inhibit the opening of the mitochondrial permeability transition pore (mPTP), a channel whose opening mediates cell death. Cardioprotection via the Reperfusion Injury Salvage Kinase (RISK) Pathway has been linked to closure of the mPTP. We hypothesized that metformin given at time of reperfusion reduces myocardial infarct size by inhibiting mPTP opening through the activation of the RISK pathway. Using perfused Wistar (non-diabetic control) and Goto-Kakizaki (a diabetic model) rat hearts, Metformin (50 μmol/L) given at time of myocardial reperfusion, reduced myocardial infarct size, effects which were abolished by the PI3K inhibitor, LY294002 (LY, 15 μmol/L). This protective effect was accompanied by Akt phosphorylation. Furthermore, metformin was found to inhibit mPTP opening in rat cardiomyocytes subjected to oxidative stress. These effects of metformin were abolished in the presence of the PI3K inhibitor, LY. Tabled 1 Group Non-diabetic I/R% Diabetic I/R% Control 62±3.0 60±3.8 Metformin *35±2.7* *43±4.7 Metformin+LY 61±6.7 56±5.7 Open table in a new tab" @default.
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- W2002907780 date "2007-06-01" @default.
- W2002907780 modified "2023-09-30" @default.
- W2002907780 title "Metformin cardioprotects the diabetic heart by inhibiting mPTP opening via the risk pathway" @default.
- W2002907780 doi "https://doi.org/10.1016/j.yjmcc.2007.03.655" @default.
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