| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10815664 | Cellular Signalling | 2012 | 7 Pages |
Abstract
⺠The extent of reperfusion injury is increased in chronic hyperlipidemic heart. ⺠The defensive preconditioning effects are abolished in hyperlipidemic heart. ⺠This would affect clinical application of preconditioning in hyperlipidemic heart. ⺠We discussed the mechanism pertaining to this context.
Keywords
SWOPPARGPI3KtetrahydrobiopterinBH4ACEPKCPPARγMPTPeNOSGSK-3βI/RMAPKROSIschemia–reperfusion injuryAngiotensin-converting enzymeAktmitochondrial permeability transition poreischemia–reperfusiontumor necrosis factor-αMyocardial protectionendothelial nitric oxide synthaseTNF-αphosphatidylinositol-3-kinaseHyperlipidemiaprotein kinase BProtein kinase Cmitogen-activated protein kinaseSecond window of protectionPreconditioningglycogen synthase kinase-3 betaReactive oxygen speciesperoxisome proliferator-activated receptor γ
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Authors
Pitchai Balakumar, Lalita Babbar,