| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10816455 | Cellular Signalling | 2012 | 7 Pages |
Abstract
⺠The acutely diabetic myocardium is resistant to ischemic injury because of the existence of 'metabolic preconditioning'. ⺠The preconditioning effects, however, are blunted in the chronically diabetic myocardium. ⺠The extent of myocardial reperfusion injury is increased in the chronically diabetic myocardium. ⺠We discussed the discrepancies on the modulatory role of diabetes mellitus in I/R-induced myocardial injury. ⺠We addressed mechanistically the attenuated cardioprotective effects of preconditioning in the diabetic heart.
Keywords
MPTPPKBIPCPKCERK 1/2HSP27c-Jun-N-terminal kinaseSTZHemeoxygenase-1pharmacological preconditioningCGRPPPARγSWOPBMK1JnkPTKPPCHO-1ICAM-1eNOSAkt/Protein kinase BI/RMAPKischemic preconditioningIschemia–reperfusion injurystreptozotocinmitochondrial permeability transition poreischemia–reperfusiontumor necrosis factor-alphaTyrosine kinaseCardioprotectionDiabetes mellitusendothelial nitric oxide synthaseTNF-αintercellular adhesion molecule-1Nitric oxideProtein tyrosine kinaseHeat shock protein 27Protein kinase Cmitogen-activated protein kinaseSecond window of protectioncalcitonin gene-related peptidePreconditioningperoxisome proliferator activated receptor γ
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Authors
Pitchai Balakumar, Nidhi Krishan Sharma,