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Titolo:
Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of G alpha(q)/G alpha(11) in cardiomyocytes
Autore:
Wettschureck, N; Rutten, H; Zywietz, A; Gehring, D; Wilkie, TM; Chen, J; Chien, KR; Offermanns, S;
Indirizzi:
Univ Heidelberg, Inst Pharmacol, D-6900 Heidelberg, Germany Univ Heidelberg Heidelberg Germany D-6900 ol, D-6900 Heidelberg, Germany Aventis Pharma, DG Cardiovasc, Frankfurt, Germany Aventis Pharma Frankfurt Germany rma, DG Cardiovasc, Frankfurt, Germany Univ Texas, SW Med Ctr, Dept Pharmacol, Dallas, TX 75235 USA Univ Texas Dallas TX USA 75235 Ctr, Dept Pharmacol, Dallas, TX 75235 USA Univ Calif San Diego, Inst Mol Med, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 ol Med, La Jolla, CA 92093 USA
Titolo Testata:
NATURE MEDICINE
fascicolo: 11, volume: 7, anno: 2001,
pagine: 1236 - 1240
SICI:
1078-8956(200111)7:11<1236:AOPOIM>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC-HYPERTROPHY; MICE; RECEPTOR; EXPRESSION; FAILURE; OVEREXPRESSION; CARDIOMYOPATHY; MYOCYTES; PATHWAYS; GROWTH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Offermanns, S Univ Heidelberg, Inst Pharmacol, D-6900 Heidelberg, Germany Univ Heidelberg Heidelberg Germany D-6900 delberg, Germany
Citazione:
N. Wettschureck et al., "Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of G alpha(q)/G alpha(11) in cardiomyocytes", NAT MED, 7(11), 2001, pp. 1236-1240

Abstract

Myocardial hypertrophy is an adaptational response of the heart to increased work load, but it is also associated with a high risk of cardiac mortality(1-3) due to its established role in the development of cardiac failure, one of the leading causes of death in developed countries. Multiple growth factors(2,3) and various downstream signaling pathways involving, for example, ras', gp-130 (ref. 4), JNK/p38 (refs. 5,6) and calcineurin/NFAT/CaM-kinase(7) have been implicated in the hypertrophic response. However, there isevidence that the initial phase in the development of myocardial hypertrophy involves the formation of cardiac para- and/or autocrine factors like endothelin-1, norepinephrine or angiotensin II (refs. 7,8), the receptors of which are coupled to G-proteins of the G(q/11)-, G(12/13)- and G(i/o)-families(5,6,8). Cardiomyocyte-specific transgenic overexpression of alpha (1)-adrenergic or angiotensin (AT(1))-receptors as well as of the G(q) alpha -subunit, G alpha (q), results in myocardial hypertrophy(9-12). These data demonstrate that chronic activation of the G(q)/G(11)-family is sufficient to induce myocardial hypertrophy. In order to test whether G(q)/G(11) mediate the physiological hypertrophy response to pressure overload, we generated amouse line lacking both G alpha (q) and G alpha (11) in cardiomyocytes. These mice showed no detectable ventricular hypertrophy in response to pressure-overload induced by aortic constriction. The complete lack of a hypertrophic response proves that the G(q)/G(11)-mediated pathway is essential for cardiac hypertrophy induced by pressure overload and makes this signaling process an interesting target for interventions to prevent myocardial hypertrophy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/05/20 alle ore 15:15:29