| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8473958 | Journal of Molecular and Cellular Cardiology | 2016 | 10 Pages |
Abstract
Thus, intrinsic activation of AMPK is critical to prevent excess mitochondrial reactive oxygen production and consequent JNK signaling during reperfusion, thereby protecting against mPTP opening, irreversible mitochondrial damage and myocardial injury.
Keywords
rPPSOD2MKK4AMPKFCCPantimycin AMPTPOCRTTCNRFoligomycinGAPDHTMRMLVDPmCATJnkTrxR2C-jun terminal kinaseAMP-activated protein kinaseMAPKROSoligomitochondrial permeability transition poreIschemiaischemia–reperfusionLeft ventricular developed pressureTriphenyl Tetrazolium ChlorideThioredoxin reductase 2ReperfusionMIFcalcium retention capacityMacrophage migration inhibitory factorLADtetramethylrhodamine methyl esterRate pressure productmitogen activated kinaseMitochondriaOxygen consumption rateswild typeSignal transductionleft anterior descending coronary arteryCRCcarbonyl cyanide 4-(trifluoromethoxy)phenylhydrazoneglyceraldehyde 3-phosphate dehydrogenaseReactive oxygen species
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Authors
Vlad G. Zaha, Dake Qi, Kevin N. Su, Monica Palmeri, Hui-Young Lee, Xiaoyue Hu, Xiaohong Wu, Gerald I. Shulman, Peter S. Rabinovitch, Raymond R. 3rd, Lawrence H. Young,