title: Scar wars: is TGFbeta the phantom menace in scleroderma?
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-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.
authors.affiliation: 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
authors.forename: Andrew
authors.initials: A
authors.lastname: Leask
mesh_terms: 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*
chemical_list: D016207:Cytokines; D051785:Smad Proteins; D016212:Transforming Growth Factor beta