We have located links that may give you full text access.
JOURNAL ARTICLE
REVIEW
Mechanisms and consequences of fibrosis in systemic sclerosis.
Nature Clinical Practice. Rheumatology 2006 March
Systemic sclerosis (SSc), also known as scleroderma, is a complex connective tissue disease that is associated with a high mortality and is challenging to treat because of its clinical heterogeneity and a lack of effective antifibrotic therapies. SSc has vascular, immunologic and fibrotic components that are pathologically interconnected. A growing understanding of the molecular and cellular mechanisms that underlie SSc pathogenesis provides logical and novel approaches to treatment. At present most therapies are organ-based. Vascular and inflammatory components of the disease can also be treated, but effective antifibrotic therapies are lacking. A number of key molecular mediators have the potential to alter immune-cell, vascular and fibrotic processes and these mediators, which include transforming growth factor-beta isoforms, endothelin-1, connective-tissue growth factor, chemokines and members of the interleukin family, are attractive targets for therapeutic modulation. Key mediators can be blocked using antibodies, soluble receptors, endogenous inhibitors or small-molecule antagonists of ligands, receptors or signaling intermediates. Overall, this is an exciting time for new therapies in SSc and advances are being made in synchrony with an improved understanding of the molecular and biochemical basis of the disease.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app