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Titolo:
Fibrinolytic system, metalloproteinases and vascular diseases
Autore:
Nalbone, G; Alessi, MC; Juhan-Vague, I;
Indirizzi:
Fac Med Timone, F-13385 Marseille, France Fac Med Timone Marseille France F-13385 imone, F-13385 Marseille, France
Titolo Testata:
M S-MEDECINE SCIENCES
fascicolo: 2, volume: 17, anno: 2001,
pagine: 170 - 176
SICI:
0767-0974(200102)17:2<170:FSMAVD>2.0.ZU;2-D
Fonte:
ISI
Lingua:
FRE
Soggetto:
PLASMINOGEN-ACTIVATOR INHIBITOR-1; ARTERIAL NEOINTIMA FORMATION; MUSCLE CELL-MIGRATION; MATRIX METALLOPROTEINASES; DEFICIENT MICE; TRANSPLANT ARTERIOSCLEROSIS; GENE-TRANSFER; EXPRESSION; ANEURYSM; ATHEROSCLEROSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Juhan-Vague, I Fac Med Timone, EPI 99-36,27 Blvd Jean Moulin, F-13385 Marseille, France Fac Med Timone EPI 99-36,27 Blvd Jean Moulin Marseille France F-13385
Citazione:
G. Nalbone et al., "Fibrinolytic system, metalloproteinases and vascular diseases", M S-MED SCI, 17(2), 2001, pp. 170-176

Abstract

Several experimental data obtained from gene invalidation in mice submitted to various vascular injury models (electrical arterial lesion, graft, genetic-induced artherosclerosis) suggest that the interaction between the fibrinolytic and metalloproteinase systems is critical in the development of vascular diseases. Besides its fundamental function to regulate intravascular thrombolysis, the fibrinolytic system is also intimately involved in the regulation of the matrix: turnover in the vessel wall and controls in this way important cellular events, such as adhesion, mig-ration and proliferation. This is achieved either directly through the action of plasmin on some matrix proteins such as laminin or fibronectin, or indirectly through the activation of the majority of pro-MMP into active MMP that degrade matrix proteins (laminin, collagene, elastin, gelatin...). PAI-1, independently of its antifibrinolytic property, also directly regulates adhesion and migration processes. These processes are involved in (re)stenosis and in plaque rupture, by acting more specifically on leukocyte infiltration, smooth muscle cell mig-ration, degradation of internal elastic lamina and angiogenesis. Promising therapeutical approaches designed to limit pericellular proteolysis in arterial wall, involve gene transfer therapy and also the class of HMG-CoA reductase inhibitors (statins) that directly regulate the expression of some genes involved in this process.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 03:32:01