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Titolo:
Novel approaches to treating cardiovascular disease: lessons from Tangier disease
Autore:
Oram, JF;
Indirizzi:
Univ Washington, Dept Med, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 ton, Dept Med, Seattle, WA 98195 USA
Titolo Testata:
EXPERT OPINION ON INVESTIGATIONAL DRUGS
fascicolo: 3, volume: 10, anno: 2001,
pagine: 427 - 438
SICI:
1354-3784(200103)10:3<427:NATTCD>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
HIGH-DENSITY-LIPOPROTEIN; CELLULAR CHOLESTEROL EFFLUX; ATP-BINDING CASSETTE; APOLIPOPROTEIN-A-I; CORONARY HEART-DISEASE; FAMILIAL HDL DEFICIENCY; ELECTRON-MICROSCOPY; ABC TRANSPORTERS; MEDIATED REMOVAL; PLASMA-MEMBRANE;
Keywords:
ABCA1; apolipoproteins; cardiovascular disease; cholesterol; familial HDL deficiency; high density lipoprotein; Tangier disease;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
77
Recensione:
Indirizzi per estratti:
Indirizzo: Oram, JF Univ Washington, Dept Med, Box 356426, Seattle, WA 98195 USA UnivWashington Box 356426 Seattle WA USA 98195 tle, WA 98195 USA
Citazione:
J.F. Oram, "Novel approaches to treating cardiovascular disease: lessons from Tangier disease", EXPERT OP I, 10(3), 2001, pp. 427-438

Abstract

Atherosclerotic cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in Western societies. Although cholesterol is a major CVD risk; factor, therapeutic interventions to loa er plasma cholesterollevels have had limited success in reducing coronary events. Thus, novel approaches are needed to reduce or eliminate CVD. A potential therapeutic target is a newly discovered ATP binding cassette transporter called ABCA1 a cell membrane protein that is the gateway for secretion of excess cholesterol from macrophages into the high density lipoprotein (HDL) metabolic pathway. Mutations in ABCA1 cause Tangier disease, a severe HDL deficiency syndrome characterised by accumulation of cholesterol in tissue macrophages and prevalent atherosclerosis. Studies of Tangier disease heterozygotes revealed that the relative activity of ABCA1 determines plasma HDL levels and susceptibility to CVD. Drugs that induce ABCA1 in mice increase clearance of cholesterol from tissues and inhibit intestinal absorption of dietary cholesterol. Thus, ABCA1-stimulating drugs have the potential to both mobilise cholesterol from atherosclerotic lesions and eliminate cholesterol from the body. By reducing plaque formation and rupture independently of the atherogenic factors involved, these drugs would be powerful agents fur treating CVD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/06/20 alle ore 01:56:20