Scar wars:: is TGFβ the phantom menace in scleroderma?

被引：44

作者：

Leask, Andrew ^{[1
]}

机构：

[1] Univ Western Ontario, Schulich Sch Med & Dent, Dept Physiol & Pharmacol, CIHR Grp Skeletal Dev & Remodeling,Div Oral Biol, London, ON N6A 5C1, Canada

来源：

ARTHRITIS RESEARCH & THERAPY | 2006年 / 8卷 / 04期

关键词：

D O I：

10.1186/ar1976

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The autoimmune disease scleroderma ( systemic sclerosis (SSc)) is characterized by extensive tissue fibrosis, causing significant morbidity. There is no therapy for the fibrosis observed in SSc; indeed, the underlying cause of the scarring observed in this disease is unknown. Transforming growth factor-beta (TGF beta) has long been hypothesized to be a major contributor to pathological fibrotic diseases, including SSc. Recently, the signaling pathways through which TGF beta activates a fibrotic program have been elucidated and, as a consequence, several possible points for anti-fibrotic drug intervention in SSc have emerged.

引用

页数：7

共 76 条

[1] Impaired Smad7-Smurf-mediated negative regulation of TGF-β signaling in scleroderma fibroblasts [J].

Asano, Y ;

Ihn, H ;

Yamane, K ;

Kubo, M ;

Tamaki, K .

JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (02) :253-264

[2] Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response [J].

Ashcroft, GS ;

Yang, X ;

Glick, AB ;

Weinstein, M ;

Letterio, JJ ;

Mizel, DE ;

Anzano, M ;

Greenwell-Wild, T ;

Wahl, SM ;

Deng, CX ;

Roberts, AB .

NATURE CELL BIOLOGY, 1999, 1 (05) :260-266

[3]

Babic AM, 1999, MOL CELL BIOL, V19, P2958

[4] Liver extracellular matrix in health and disease [J].

Bedossa, P ;

Paradis, V .

JOURNAL OF PATHOLOGY, 2003, 200 (04) :504-515

[5] THE MODULAR ARCHITECTURE OF A NEW FAMILY OF GROWTH-REGULATORS RELATED TO CONNECTIVE-TISSUE GROWTH-FACTOR [J].

BORK, P .

FEBS LETTERS, 1993, 327 (02) :125-130

[6] The loss of Smad3 results in a lower rate of bone formation and osteopenia through dysregulation of osteoblast differentiation and apoptosis [J].

Borton, AJ ;

Frederick, JP ;

Datto, MB ;

Wang, XF ;

Weinstein, RS .

JOURNAL OF BONE AND MINERAL RESEARCH, 2001, 16 (10) :1754-1764

[7] Biology of TGF-beta in knockout and transgenic mouse models [J].

Bottinger, EP ;

Letterio, JJ ;

Roberts, AB .

KIDNEY INTERNATIONAL, 1997, 51 (05) :1355-1360

[8] CTGF expression in mesangial cells: Involvement of SMADs, MAP kinase, and PKC [J].

Chen, YJ ;

Blom, IE ;

Sa, S ;

Goldschmeding, R ;

Abraham, DJ ;

Leask, A .

KIDNEY INTERNATIONAL, 2002, 62 (04) :1149-1159

[9] Contribution of activin receptor-like kinase 5 (Transforming growth factor β receptor type I) signaling to the fibrotic phenotype of scleroderma fibroblasts [J].

Chen, YL ;

Xu, SW ;

Eastwood, M ;

Black, CM ;

Denton, CP ;

Leask, A ;

Abraham, DJ .

ARTHRITIS AND RHEUMATISM, 2006, 54 (04) :1309-1316

[10] Matrix contraction by dermal fibroblasts requires transforming growth factor-β/activin-linked kinase 5, heparan sulfate-containing proteoglycans, and MEK/ERK -: Insights into pathological scarring in chronic fibrotic disease [J].

Chen, YL ;

Xu, SW ;

van Beek, J ;

Kennedy, L ;

McLeod, M ;

Renzoni, EA ;

Bou-Gharios, G ;

Wilcox-Adelman, S ;

Goetinck, PF ;

Eastwood, M ;

Black, CM ;

Abraham, DJ ;

Leask, A .

AMERICAN JOURNAL OF PATHOLOGY, 2005, 167 (06) :1699-1711

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