Journal
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY
Volume 48, Issue -, Pages 569-599Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.pharmtox.48.121806.154902
Keywords
atherosclerosis; fibrosis; hypertrophy; heart failure; protein kinase C; signal transduction; rational drug design; novel therapeutics
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL076675] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL 76675] Funding Source: Medline
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Cardiovascular disease is the leading cause of death in the United States. Therefore, identifying therapeutic targets is a major focus of current research. Protein kinase C (PKC), a family of serine/threonine kinases, has been identified as playing a role in many of the pathologies of heart disease. However, the lack of specific PKC regulators and the ubiquitous expression and normal physiological functions of the 11 PKC isozymes has made drug development a challenge. Here we discuss the validity of therapeutically targeting PKC, an intracellular signaling enzyme. We describe PKC structure, function, and distribution in the healthy and diseased heart, as well as the development of rationally designed isozyme-selective regulators of PKC functions. The review focuses on the roles of specific PKC isozymes in atherosclerosis, fibrosis, and cardiac hypertrophy, and examines principles of pharmacology as they pertain to regulators of signaling cascades associated with these diseases.
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