A. Clerk et Ph. Sugden, Activation of protein kinase cascades in the heart by hypertrophic G protein-coupled receptor agonists, AM J CARD, 83(12A), 1999, pp. 64H-69H
Citations number
66
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Cardiac myocyte hypertrophy involves changes in cell structure and alterati
ons in protein expression regulated at both the transcriptional and transla
tional levels. Hypertrophic G protein-coupled receptor (GPCR) agonists such
as endothelin-1 (ET-1) and phenylephrine stimulate a number of protein kin
ase cascades in the heart. Mitogen-activated protein kinase (MAPK) cascades
stimulated include the extracellularly regulated kinase cascade, the stres
s-activated protein kinase/c-Jun N-terminal kinase cascade, and the p38 MAP
K cascade. All 3 pathways have been implicated in hypertrophy, but recent e
x vivo evidence also suggests that there may be additional effects on cell
survival. ET-1 and phenylephrine also stimulate the protein kinase B pathwa
y, and this may be involved in the regulation of protein synthesis by these
agonists, Thus, protein kinase-mediated signaling may be important in the
regulation of the development of myocyte hypertrophy. (C)1999 by Excerpta M
edica, Inc.