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Titolo:
Quantitative and qualitative anomalies of LDL: relevance to atherosclerosis
Autore:
Chapman, JM; Guerin, M; Bruckert, E;
Indirizzi:
CHU Pitie Salpetriere, INSERM U321, F-75651 Paris 13, France CHU Pitie Salpetriere Paris France 13 ERM U321, F-75651 Paris 13, France
Titolo Testata:
BULLETIN DE L ACADEMIE NATIONALE DE MEDECINE
fascicolo: 1, volume: 185, anno: 2001,
pagine: 35 - 39
SICI:
0001-4079(2001)185:1<35:QAQAOL>2.0.ZU;2-S
Fonte:
ISI
Lingua:
FRE
Keywords:
arterioscleriosclerosis; hypercholesterolemia, therapy; receptors, cell surface; lipoproteins, LDL; lipoproteins, LLDL; apolipoproteins B;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
0
Recensione:
Indirizzi per estratti:
Indirizzo: Chapman, JM CHU Pitie Salpetriere, INSERM U321, Pavillon B Delessert,83 Bld Hop, F-75651 Paris 13, France CHU Pitie Salpetriere Pavillon B Delessert,83 Bld Hop Paris France 13
Citazione:
J.M. Chapman et al., "Quantitative and qualitative anomalies of LDL: relevance to atherosclerosis", B ACA N MED, 185(1), 2001, pp. 35-39

Abstract

Qualitative and quantitative anomalies of low-density lipoproteins (LDL) play a key role in the pathophysiology of atherosclerosis. Such anomalies are characteristic of the atherogenic dyslipidemias which occur most frequently, ie. primary hypercholesterolemia of phenotype IIA (including familial hypercholesterolemia), combined hyperlipidemias (Type IIB) and hypertriglyceridemia (Type IV). An elevated concentration of circulating LDL occurs either as a result of hepatic overproduction of VLDL particles, the major precussors of LDL, or asa result of delayed catabolism, as occurs when there is a deficit of cellular LDL receptors (eg. familial hypercholesterolemia), oras a combination of both, The major qualitative anomaly of LDL which results in elevated atherogenicity involves a predominance of small dense LDL, as seen in patients with premature coronary heart disease and equally in combined hyperlipidemia and in The mechanism of the formation of these particles is complex and involves the cancer ted intravascular action of cholesteryl ester transfer protein (CETP), lipoprotein lipase (LPL) and hepatic lipase (HL) on triglyceride-rich precursors of dense LDL Lipid-lowering agents,such as fibrates and statins, act to reduce the atherogenicity of dense LDL by distinct mechanisms, which lead to normalisation of circulating LDL levels and/or to targeted reduction in dense particles of elevated atherogenicity. Indeed, such pharmacological probes have facilitated new insight intothe molecular and cellular,mechanisms which underlie each of the major forms of atherogenic dyslipidemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 19:27:04