Copyright © 2006, European Society of Cardiology
Epsilon protein kinase C as a potential therapeutic target for the ischemic heart
Department of Molecular Pharmacology, Stanford University School of Medicine, CCSR, Room 3145A, 269 Campus Drive Stanford, CA 94305-5174, United States
* Correspondence author. Tel.: +1 650 725 7720; fax: +1 650 723 2253. Email address: mochly{at}stanford.edu
Ischemic heart disease is the leading cause of morbidity and mortality in the western world. Ischemic damage can occur by acute myocardial infarction, stable angina, cardiac stunning, and myocardial hibernation. In addition, ‘scheduled’ ischemic events, occurring during cardiac surgery, heart transplantation, and elective angioplasty, can also result in cardiac damage. Ischemic or pharmacological preconditioning can decrease the extent of damage to the myocardium. Although the mechanism of preconditioning-mediated cardioprotection is not fully understood, 
PKC has been implicated as a critical mediator of this process in animal studies. The use of isozyme-specific pharmacological tools has permitted a better elucidation of the upstream stimuli and the downstream transducers of PKC in the pathways leading to cardioprotection. While little is known about the role of PKC in these pathways in humans, animal studies suggest a potential therapeutic role of PKC. This review will focus on the role of PKC in cardiac protection and on the signal transduction cascades that have been implicated in this protection.
KEYWORDS Preconditioniong; Postconditioning; Ischemia/reperfusion; PKC; ROS; KATP channel; Cardiac transplant; Signal transduction
1 DMR is the founder of KAI Pharmaceuticals, Inc, a company that plans to bring PKC regulators to the clinic. However, none of the work described in the review is based on or supported by the company.
Time for primary review 17 days
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