beta IIPKC and epsilon PKC isozymes as potential pharmacological targets in cardiac hypertrophy and heart failure

Author(s)

Batista Ferreira, Julio Cesar ^{[1, 2]} ; Brum, Patricia Chakur ^[2] ; Mochly-Rosen, Daria ^[1]

Affiliation

^[1] Stanford Univ, Sch Med, Dept Chem & Syst Biol, CCSR, Stanford, CA 94305 - USA

^[2] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508900 Sao Paulo - Brazil

• Document type: Review article
• Source: JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY; v. 51, n. 4, p. 479-484, OCT 2011.
• Web of Science Citations: 31

Abstract

Cardiac hypertrophy is a complex adaptive response to mechanical and neurohumoral stimuli and under continual stressor, it contributes to maladaptive responses, heart failure and death. Protein kinase C (PKC) and several other kinases play a role in the maladaptative cardiac responses, including cardiomyocyte hypertrophy, myocardial fibrosis and inflammation. Identifying specific therapies that regulate these kinases is a major focus of current research. PKC, a family of serine/threonine kinases, has emerged as potential mediators of hypertrophic stimuli associated with neurohumoral hyperactivity in heart failure. In this review, we describe the role of PKC isozymes that is involved in cardiac hypertrophy and heart failure. This article is part of a special issue entitled ``Key Signaling Molecules in Hypertrophy and Heart Failure{''}. (C) 2010 Elsevier Ltd. All rights reserved. (AU)

• FAPESP's process: 09/03143-1 - Protein quality control in heart failure: role of different protein kinase C isozymes
• Grantee: Julio Cesar Batista Ferreira
• Support type: Scholarships in Brazil - Post-Doctorate