Article ID Journal Published Year Pages File Type
5842877 Life Sciences 2011 8 Pages PDF
Abstract
These results demonstrate that U50,488H administered immediately prior to reperfusion increases Akt phosphorylation through a PI3-kinase-dependent mechanism and reduces postischemic myocardial apoptosis. Phosphorylation of eNOS with secondary NO production contribute significantly to the anti-apoptotic effect of U50,488H postconditioning.
Related Topics
Health Sciences Medicine and Dentistry Cardiology and Cardiovascular Medicine
Authors
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