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Cardiology Research and Practice
Volume 2012, Article ID 521958, 9 pages
Review Article

Modulation of Fibrosis in Systemic Sclerosis by Nitric Oxide and Antioxidants

1Centre for Rheumatology and Connective Tissue Disease, University College London Medical School, Royal Free Campus, London NW3 2PF, UK
2Institute of Structural and Molecular Biology, University College London Medical School, Gower Street, London WC1E 6BT, UK

Received 29 July 2011; Accepted 11 September 2011

Academic Editor: Janice Tsui

Copyright © 2012 Audrey Dooley et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Systemic sclerosis (scleroderma: SSc) is a multisystem, connective tissue disease of unknown aetiology characterized by vascular dysfunction, autoimmunity, and enhanced fibroblast activity resulting in fibrosis of the skin, heart, and lungs, and ultimately internal organ failure, and death. One of the most important and early modulators of disease activity is thought to be oxidative stress. Evidence suggests that the free radical nitric oxide (NO), a key mediator of oxidative stress, can profoundly influence the early microvasculopathy, and possibly the ensuing fibrogenic response. Animal models and human studies have also identified dietary antioxidants, such as epigallocatechin-3-gallate (EGCG), to function as a protective system against oxidative stress and fibrosis. Hence, targeting EGCG may prove a possible candidate for therapeutic treatment aimed at reducing both oxidant stress and the fibrotic effects associated with SSc.