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on January 6, 2005

Arteriosclerosis, Thrombosis, and Vascular Biology. 2005
Published online before print January 6, 2005, doi: 10.1161/01.ATV.0000155325.41507.e0
A more recent version of this article appeared on March 1, 2005
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*Substance via MeSH

Submitted on July 30, 2004
Accepted on December 27, 2004

Proatherosclerotic Mechanisms Involving Protein Kinase C in Diabetes and Insulin Resistance

Christian Rask-Madsen and George L. King *

From Joslin Diabetes Center, Harvard Medical School, Boston, Mass.

* To whom correspondence should be addressed. E-mail: george.king{at}joslin.harvard.edu.

Abstract--In diabetes and insulin resistance, activation of protein kinase C (PKC) in vascular cells may be a key link between elevated plasma and tissue concentrations of glucose and nonesterified fatty acids and abnormal vascular cell signaling. Initial studies of PKC activation in diabetes focused on microvascular complications, but increasing evidence supports that PKC plays a role in several mechanisms promoting atherosclerosis. This review explains how PKC is thought to be activated in diabetes and insulin resistance through de novo synthesis of diacylglycerol. Furthermore, the review summarizes studies that implicate PKC in promoting proatherogenic mechanisms or inhibiting antiatherogenic mechanisms, including studies of endothelial dysfunction; gene induction and activation of vascular NAD(P)H oxidase; endothelial nitric oxide synthase expression and function; endothelin-1 expression; growth, migration, and apoptosis of vascular smooth muscle cells; induction of adhesion molecules; and oxidized low-density lipoprotein uptake by monocyte-derived macrophages.




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