STATE-OF-THE-ART PAPER
Protein Kinase C ß/Early Growth Response-1 Pathway
A Key Player in Ischemia, Atherosclerosis, and Restenosis
Shi-Fang Yan, MD*,
Evis Harja, MD,
Martin Andrassy, MD,
Tomoyuki Fujita, MD and
Ann Marie Schmidt, MD
Department of Surgery, Columbia University, New York, New York.
Manuscript received March 30, 2006;
revised manuscript received May 24, 2006,
accepted May 29, 2006.
*
Reprint requests and correspondence: Dr. Shi-Fang Yan, Division of Surgical Science, Department of Surgery, College of Physicians and Surgeons of Columbia University, 630 West 168th Street, BB1705, New York, New York 10032. (Email: sy18{at}columbia.edu).
Atherosclerosis, restenosis, and the consequences of ischemia are the major causes of morbidity and mortality worldwide. Elucidation of key contributing pathways in animal models of ischemia-reperfusion injury, atherosclerosis, and restenosis consequent to vascular injury may lead to great interest in determining if blocking these pathways could prevent vascular disease in human subjects. This review details the evidence that the protein kinase C (PKC) ß/early growth response-1 axis plays a central role in the response to both acute and chronic vascular stresses in animal models and also indicates the clinical implications of a specific inhibitor of PKCß, ruboxistaurin (LY333531).
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Abbreviations and Acronyms
| | apoE = apolipoprotein E | | Egr-1 = early growth response-1 | | ERK1/2 = extracellular-signal-regulated protein kinase | | JNK = c-Jun N-terminal kinase | | OxLDL = oxidized low-density lipoprotein | | PKC = protein kinase C |
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Copyright © 2006 by the American College of Cardiology Foundation.
