scar wars is tgfβ the phantom menace in scleroderma疤痕战争是硬皮病tgfβ幽灵的威胁》.pdfVIP

Available online /content/8/4/213 Review Scar wars: is TGFββ the phantom menace in scleroderma? Andrew Leask Division 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 author: Andrew Leask, Andrew.Leask@schulich.uwo.ca Published: 9 June 2006 Arthritis Research Therapy 2006, 8:213 (doi:10.1186/ar1976) This article is online at /content/8/4/213 © 2006 BioMed Central Ltd Abstract fibrotic responses, including SSc [5]; however, the exact The autoimmune disease scleroderma (systemic sclerosis (SSc)) is contribution of TGFβ to the fibrotic phenotype of SSc is characterized by extensive tissue fibrosis, causing significant unclear. Furthermore, as TGFβ plays many roles in normal morbidity. There is no therapy for the fibrosis observed in SSc; physiology, including as a suppressor of the immune indeed, the underlying cause of the scarring observed in this response and epithelial proliferation, broadly targeting TGFβ disease is unknown. Transforming growth factor-β (TGFβ) has long signaling for the treatment of disease is anticipated to be been hypothesized to be a major contributor to pathological fibrotic problematic [8]. Thus, much interest exists, from both clinical diseases, including SSc. Recently, the signaling pathways through which TGFβ activates a fibrotic program have been elucidated and,