New Insights into the Role of Oxidative Stress in Scleroderma Fibrosis
Armando Gabrielli*, Silvia Svegliati, Gianluca Moroncini , Donatella Amico
Identifiers and Pagination:Year: 2012
Issue: Suppl 1
First Page: 87
Last Page: 95
Publisher ID: TORJ-6-87
Article History:Received Date: 3/3/2012
Revision Received Date: 27/3/2012
Acceptance Date: 4/4/2012
Electronic publication date: 15/6/2012
Collection year: 2012
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Systemic sclerosis (Scleroderma – SSc) is a connective tissue disorder of unknown aetiology characterized by extensive fibrosis of the skin and visceral organs, by vascular abnormalities and immunological manifestations.
Recent evidence suggest that the cellular redox state may play a significant role in the progression of scleroderma fibrosis. Mechanisms involved include an autoamplification circuit linking ROS, Ras and ERK 1-2 which in turn amplifies and maintains the autocrine loop made up by cytokines, growth factors and their cognate receptors.
This review summarizes the recent progress on the role of oxidative stress in the pathophysiology of scleroderma and disorders characterised by organ fibrosis