© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Signal transduction during cardiac hypertrophy: the role of G
q, PLC βI, and PKC
Department of Medicine, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106-5029, USA
* Corresponding author. Tel.: 1-216-844-3293; fax: 1-216-844-3145 raw19@po.cwru.edu
Received 6 November 1998; accepted 29 March 1999
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1 Introduction |
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Currently the precise biochemical pathogenesis of cardiac hypertrophy remains unclear. A great deal of investigation has been directed toward the examination of various signal transduction pathways that are thought to be involved in stimulating this process. In particular, the signaling pathways that use heterotrimeric G protein-coupled receptors have been the focus for many investigations. This review will focus on the function of the G
q family of proteins and its downstream effectors during cardiac hypertrophy. Hypertrophy is the final common pathway for a variety of insults to the normal cardiovascular system. Many mechanical and hormonal stimuli such as hypertension, valve disorders, and ischemic events, can produce a hypertrophic response. These pathologic stimuli cause an increase in the workload placed upon the heart resulting in hypertrophy and remodeling that has been observed at the myocyte [1] and the gross anatomical level. Current thought suggests that the hypertrophic response is a compensatory mechanism |
2 G protein-coupled receptor signaling |
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2.1 The role of G
q signaling in cardiac hypertrophy2.2 Signaling through G
q activates phospholipase c β (PLC β) and protein kinase C (PKC)2.3 Protein kinase C and cardiac hypertrophy
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3 Conclusions |
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