Cargando…

Scar wars: is TGFβ 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 fact...

Descripción completa

Detalles Bibliográficos
Autor principal: Leask, Andrew
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779423/
https://www.ncbi.nlm.nih.gov/pubmed/16774692
http://dx.doi.org/10.1186/ar1976
_version_ 1782131767311859712
author Leask, Andrew
author_facet Leask, Andrew
author_sort Leask, Andrew
collection PubMed
description 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.
format Text
id pubmed-1779423
institution National Center for Biotechnology Information
language English
publishDate 2006
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-17794232007-01-19 Scar wars: is TGFβ the phantom menace in scleroderma? Leask, Andrew Arthritis Res Ther Review 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. BioMed Central 2006 2006-06-09 /pmc/articles/PMC1779423/ /pubmed/16774692 http://dx.doi.org/10.1186/ar1976 Text en Copyright © 2006 BioMed Central Ltd
spellingShingle Review
Leask, Andrew
Scar wars: is TGFβ the phantom menace in scleroderma?
title Scar wars: is TGFβ the phantom menace in scleroderma?
title_full Scar wars: is TGFβ the phantom menace in scleroderma?
title_fullStr Scar wars: is TGFβ the phantom menace in scleroderma?
title_full_unstemmed Scar wars: is TGFβ the phantom menace in scleroderma?
title_short Scar wars: is TGFβ the phantom menace in scleroderma?
title_sort scar wars: is tgfβ the phantom menace in scleroderma?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779423/
https://www.ncbi.nlm.nih.gov/pubmed/16774692
http://dx.doi.org/10.1186/ar1976
work_keys_str_mv AT leaskandrew scarwarsistgfbthephantommenaceinscleroderma