Abstract |
Cardiac hypertrophy is an adaptive response to any cardiac insult or stress that increases hemodynamic load. Cardiac hypertrophy can exist in a state of compensation or progress to a decompensated state (i.e., heart failure) over time. It has been established through transgenic overexpression and gene ablation studies that multiple signaling pathways are involved in the induction of hypertrophy as well as its decompensation. This article reviews the role of G alpha q in the development of pressure overload hypertrophy and discusses the relationships between G alpha q and beta-adrenergic receptors, RGS proteins, and the proapoptotic factor, Nix/Bnip3L.
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Authors | Gerald W Dorn 2nd, Harvey S Hahn |
Journal | Annals of the New York Academy of Sciences
(Ann N Y Acad Sci)
Vol. 1015
Pg. 225-37
(May 2004)
ISSN: 0077-8923 [Print] United States |
PMID | 15201163
(Publication Type: Journal Article, Review)
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Chemical References |
- Protein Kinase C
- GTP-Binding Protein alpha Subunits, Gq-G11
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Topics |
- Apoptosis
(genetics)
- Cardiomegaly
(genetics, pathology, physiopathology)
- GTP-Binding Protein alpha Subunits, Gq-G11
(physiology)
- Protein Kinase C
(metabolism)
- Signal Transduction
(physiology)
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