Scar wars: is TGFbeta the phantom menace in scleroderma?
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 (TGFbeta) has long been hypothesized to be a major contributor to pathological fibrotic diseases, including SSc. Recently, the signaling pathways through which TGFbeta activates a fibrotic program have been elucidated and, as a consequence, several possible points for anti-fibrotic drug intervention in SSc have emerged.
Leask
Andrew
A
Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London, ON N6A 5C1, Canada. Leask@schulich.uwo.ca
D002921:Cicatrix / Q000209:etiology*; D016207:Cytokines / Q000378:metabolism; D004357:Drug Synergism; D005355:Fibrosis; D006801:Humans; D012595:Scleroderma, Systemic / Q000150:complications* / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051785:Smad Proteins / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism*
D016207:Cytokines; D051785:Smad Proteins; D016212:Transforming Growth Factor beta