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Insulin therapy as an adjunct toreperfusion after acute coronary ischemia

A proposed direct myocardial cell survival effect independent of metabolic modulation

Michael N. Sack, MD, PhD^* and Derek M. Yellon, PhD, DSc, Hon FRCP, FACC^,*

^* The Hatter Institute for Cardiology Research, MRC Inter-University Cape Heart Group, University of Cape Town Medical School, Cape Town, South Africa
The Hatter Institute for Cardiovascular Studies, UCL Hospitals & Medical School, London, United Kingdom

View larger version (27K): [in a new window]   Figure 1 Schematic of insulin signaling pathways that promote cell survival and facilitate increased glucose uptake. These signaling pathways have recently been reviewed in depth. Akt = protein kinase B; BAD = Bcl-2/Bcl-XL-agonist causing cell death; eNOS = endothelial nitric oxide synthase; PI3K = phosphatidylinositol 3,4,5-trisphosphate; S6K = p70S6 kinase (70-kDa ribosomal protein S6 kinase). The superscripted p denotes the phosphorylation status of BAD and eNOS, respectively.