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Arthritis Res Ther. 2006; 8(4): 213.
Published online Jun 9, 2006. doi:  10.1186/ar1976
PMCID: PMC1779423
Scar wars: is TGFβ the phantom menace in scleroderma?
Andrew Leaskcorresponding author1
1Division of Oral Biology and Department of Physiology and Pharmacology, CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London, ON N6A 5C1, Canada
corresponding authorCorresponding author.
Andrew Leask: Leask/at/schulich.uwo.ca
Abstract
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-β (TGFβ) has long been hypothesized to be a major contributor to pathological fibrotic diseases, including SSc. Recently, the signaling pathways through which TGFβ activates a fibrotic program have been elucidated and, as a consequence, several possible points for anti-fibrotic drug intervention in SSc have emerged.
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