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Titolo:
Cellular and molecular biology of atherosclerotic lesions
Autore:
Martinez-Gonzalez, J; Llorente-Cortes, V; Badimon, L;
Indirizzi:
Hosp Santa Cruz & San Pablo, Inst Recerca, CSIC, IIBB,Ctr Invest Cardiovasc, E-08025 Barcelona, Spain Hosp Santa Cruz & San Pablo Barcelona Spain E-08025 025 Barcelona, Spain
Titolo Testata:
REVISTA ESPANOLA DE CARDIOLOGIA
fascicolo: 2, volume: 54, anno: 2001,
pagine: 218 - 231
SICI:
0300-8932(200102)54:2<218:CAMBOA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
SPA
Soggetto:
SMOOTH-MUSCLE CELLS; LOW-DENSITY-LIPOPROTEIN; NITRIC-OXIDE-SYNTHASE; CORONARY-ARTERY DISEASE; FACTOR-KAPPA-B; PLASMINOGEN-ACTIVATOR INHIBITOR-1; AVERAGE CHOLESTEROL LEVELS; COA REDUCTASE INHIBITORS; ENDOTHELIAL-CELLS; GENE-EXPRESSION;
Keywords:
atherosclerosis; smooth muscle cells (CML); low density lipoproteins (LDL); macrophages;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
107
Recensione:
Indirizzi per estratti:
Indirizzo: Badimon, L CSIC, IIBB, Jordi Girona 18-26, Barcelona 08034, Spain CSIC Jordi Girona 18-26 Barcelona Spain 08034 ona 08034, Spain
Citazione:
J. Martinez-Gonzalez et al., "Cellular and molecular biology of atherosclerotic lesions", REV ESP CAR, 54(2), 2001, pp. 218-231

Abstract

The association of atherosclerosis with the most common risk factors including elevation of low density lipoprotein (LDL) levels. diabetes, hypertension and cigarette smoking, led to the hypothesis of <<response to injury>>,td explain how the lesions develop. According to this hypothesis, one of the earliest events in atherogenesis is the accumulation of LDL in the arterial wall where they undergo oxidation. These LDL impair endothelial function, and thus, all the antiatherogenic properties of the endothelium. in addition, macrophages and smooth muscle cells take up these LDL, through different receptors, and become foam cells. The accumulation of foam cells in thearterial wall contributes to lesion development. Therefore, lesion development involves the activation of endothelial cells, as well as smooth musclecells and monocytes/macrophages. In this activation different growth factors (PDGF, EGF, etc.), cytokines (IL-1 beta, TNF alpha, etc.) and the modified LDL themselves, play an important role. Through several signal transduction pathways these molecules activate transcription factors, such as the nuclear factor kappa B (NF-kappaB) or protooncogenes such asc-fos, c-myc, that regulate the expression of genes involved in the inflammatory/proliferative response of the lesions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 19:34:51