Scar wars: is TGFbeta the phantom menace in scleroderma?

Arthritis Res Ther. 2006;8(4):213. doi: 10.1186/ar1976.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cicatrix / etiology*
  • Cytokines / metabolism
  • Drug Synergism
  • Fibrosis
  • Humans
  • Scleroderma, Systemic / complications*
  • Scleroderma, Systemic / genetics
  • Scleroderma, Systemic / metabolism*
  • Scleroderma, Systemic / pathology
  • Smad Proteins / metabolism
  • Transforming Growth Factor beta / metabolism*


  • Cytokines
  • Smad Proteins
  • Transforming Growth Factor beta