کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10816994 | 1058623 | 2008 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Targeting the TGFβ, endothelin-1 and CCN2 axis to combat fibrosis in scleroderma
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Targeting the TGFβ, endothelin-1 and CCN2 axis to combat fibrosis in scleroderma Targeting the TGFβ, endothelin-1 and CCN2 axis to combat fibrosis in scleroderma](/preview/png/10816994.png)
چکیده انگلیسی
Fibrosis affects organs such as the skin, liver, kidney and lung and is a cause of significant morbidity. There is no therapy for fibrosis. Recent significant molecular insights into the signaling underlying the fibrosis in the autoimmune connective tissue disease scleroderma (systemic sclerosis, SSc) have been made. Transforming growth factor β (TGFβ) signaling is a major contributor to fibrogenesis, including in SSc. However, it is now appreciated that TGFβ-dependent and TGFβ-independent mechanisms play key roles in the pathological fibrosis in SSc. In particular the potent pro-fibrotic proteins endothelin-1 (ET-1) and CCN2 (connective tissue growth factor, CTGF) are believed to play an essential role in this process. This review summarizes these recent crucial observations.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 20, Issue 8, August 2008, Pages 1409-1414
Journal: Cellular Signalling - Volume 20, Issue 8, August 2008, Pages 1409-1414
نویسندگان
Andrew Leask,