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Oxidative stress is important in the pathogenesis of lung fibrosis in scleroderma

Posted Sep 11 2009 4:58pm

The research about "Analysis of bronchoalveolar lavage fluid proteome from systemic sclerosis patients with or without functional, clinical and radiological signs of lung fibrosis" by AM Fietta and colleague shows that the several factors, including activation of the coagulation cascade and oxidative stress, are thought to influence the development of lung fibrosis.

The antioxidant enzymes such as glutathione S-transferase P (GSTP)and Cu–Zn superoxide dismutase (SOD) of scleroderma's patients are decrease because they are used in the protection cell from oxidative stress (Ex. ROS, reactive oxygen species; RNS, reactive nitrogen species; O2-, superoxide; H2O2, hydrogen peroxide and NO, nitric oxide).



"Hypothetical role of some disregulated BALf proteins in mechanisms driving SSc-related lung fibrosis. Inflammation is thought to be the main mechanism driving lung fibrosis in scleroderma patients. In this complex inflammatory process several pathways are involved, including the activation of T cells and epithelial cells, the secretion of pro-inflammatory cytokines and growth factors, and fibroblast proliferation. Furthermore, products from the coagulation cascade and oxidative stress may contribute to fibrogenesis. The upregulation of calgranulin B (Cal B), cytohesin-2 and calumenin might favor inflammation and fibrogenesis, whereas the downmodulation of the protective factors glutathione S-transferase P (GSTP), Cu–Zn superoxide dismutase (SOD) and cystatin SN may amplify tissue injury and inflammation. MMP, matrix metalloproteinases; TIMP, tissue inhibitor of matrix metalloproteinases; ROS, reactive oxygen species; RNS, reactive nitrogen species; O2-, superoxide; H2O2, hydrogen peroxide; NO, nitric oxide; SScFib+, systemic sclerosis patients with lung fibrosis; SScFib-, systemic sclerosis patients without lung fibrosis."

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