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Titolo:
Role of sodium-hydrogen exchange in cardiac hypertrophy and heart failure:a novel and promising therapeutic target
Autore:
Karmazyn, M;
Indirizzi:
Univ Western Ontario, Dept Pharmacol & Toxicol, London, ON N6A 5C1, CanadaUniv Western Ontario London ON Canada N6A 5C1 London, ON N6A 5C1, Canada
Titolo Testata:
BASIC RESEARCH IN CARDIOLOGY
fascicolo: 4, volume: 96, anno: 2001,
pagine: 325 - 328
SICI:
0300-8428(200107)96:4<325:ROSEIC>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
NA+-H+ EXCHANGE; STRETCH; ANGIOTENSIN; AMILORIDE; MYOCYTES; BLOCKER; MUSCLE;
Keywords:
NHE-1; hypertrophy; remodelling; heart failure; Na+/H+ exchange;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
17
Recensione:
Indirizzi per estratti:
Indirizzo: Karmazyn, M Univ Western Ontario, Dept Pharmacol & Toxicol, Med Sci Bldg, London, ON N6A 5C1, Canada Univ Western Ontario Med Sci Bldg London ON Canada N6A 5C1 ada
Citazione:
M. Karmazyn, "Role of sodium-hydrogen exchange in cardiac hypertrophy and heart failure:a novel and promising therapeutic target", BAS R CARD, 96(4), 2001, pp. 325-328

Abstract

The myocardial sodium-hydrogen exchanger (NHE), and more specifically the NHE-1 isoform is now well-recognized to be a major contributor to ischemic and reperfusion injury. Recent evidence suggests that NHE-1 is also potential candidate for targeted intervention in terms of attenuation of the remodelling and hypertrophic processes which contributes to heart failure. Experimental studies have shown that NHE-1 inhibitors attenuate cardiomyocyte hypertrophy induced by various factors and reduce heart failure in vivo, independently of infarct size reduction. Although the precise cellular mechanisms for NHE-1 involvement remain to be elucidated, current data suggest a potentially effective new therapeutic approach for the treatment of heart failure via NHE-1 inhibition.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 20:05:17