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Titolo:
Transforming growth factor-beta and connective tissue growth factor: key cytokines in scleroderma pathogenesis
Autore:
Denton, CP; Abraham, DJ;
Indirizzi:
Royal Free & Univ Coll Med Sch, Ctr Rheumatol, London NW3 2QG, England Royal Free & Univ Coll Med Sch London England NW3 2QG n NW3 2QG, England
Titolo Testata:
CURRENT OPINION IN RHEUMATOLOGY
fascicolo: 6, volume: 13, anno: 2001,
pagine: 505 - 511
SICI:
1040-8711(200111)13:6<505:TGFACT>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
IDIOPATHIC PULMONARY FIBROSIS; FACTOR GENE-EXPRESSION; INDUCED LUNG FIBROSIS; TIGHT-SKIN MOUSE; SYSTEMIC-SCLEROSIS; TGF-BETA; I PROCOLLAGEN; ASSOCIATION; RECEPTOR; FIBROBLASTS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Denton, CP Royal Free & Univ Coll Med Sch, Ctr Rheumatol, Rowland Hill St,London NW32QG, England Royal Free & Univ Coll Med Sch Rowland Hill St London England NW3 2QG
Citazione:
C.P. Denton e D.J. Abraham, "Transforming growth factor-beta and connective tissue growth factor: key cytokines in scleroderma pathogenesis", CURR OP RH, 13(6), 2001, pp. 505-511

Abstract

Evidence for a role for members of the transforming growth factor beta (TGF-beta) family of cytokines in the pathogenesis of systemic sclerosis and other fibrotic conditions is provided from studies of TGF-beta protein and gene expression in lesional biopsy specimens, from altered responses of explanted fibroblasts to TGF-beta stimulation which are associated with increased receptor expression on these cells and from genetic data linking TGF-beta gene loci to the disease. Of the many effects of TGF-beta on fibroblast properties induction of the connective tissue growth factor/Cyr61/NOV (CCN) family members, connective tissue growth factor (CTGF) may be particularly relevant to fibrosis. Moreover, systemic sclerosis (SSc) fibroblasts demonstrate constitutive over expression of CTGF that promotes migration, proliferation and matrix production. Studies of mechanisms regulating constitutiveexpression of CTGF by SSc fibroblasts are currently being undertaken and indicate that a TGF-beta responsive element in the CTGF promoter is involved, although this appears to function independent of the Smad proteins, suggesting that other TGF-beta -regulated pathways may be involved. TGF-neutralizing strategies have now been shown to abrogate many animal models of fibrosis, and will soon reach the clinical arena for SSc. These agents will further clarify the role of this ligand in initiating or sustaining fibrosis and offer the exciting possibility of targeted therapy for this disease. CurrOpin Rheumatol 2001, 13:505-511 (C) 2001 Lippincott Williams & Wilkins, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 22:32:49