Pathogenetic role of oxidative stress in Localized scleroderma

Abstract

Annotation. Localized scleroderma has a progressive, disabling course and complex pathogenetic mechanisms. It is important to assess the effect of oxidative stress on the content of pro-inflammatory cytokines and the activity of fibrosis. Sources were searched using PubMed and Google Scholar using keywords and abbreviations: Localized scleroderma, pathophysiology, oxidative stress, reactive oxygen species. Search results are processed by methods of survey, system and content analysis. It is set that the basis of the pathogenesis of the disease are three interdependent processes: the defeat of small arterioles and capillaries, immune disorders, excess collagen production by fibroblasts. In Localized scleroderma, there is an increase in the processes of free radical oxidation of lipids with increasing activity of the total oxidative capacity of blood serum. Reactive forms of oxygen (ROS) cause a number of disorders: oxidative damage to DNA, endothelial cells, increased platelet activation with abnormal expression of adhesion molecules and secretion of fibrogenic proinflammatory cytokines. Experimental studies have shown the ability of ROS to enhance the production of TGF-β, collagen and a marker of myofibroblasts – α-SM. The leading role is played by pathological activation of fibroblasts, which leads to the disposition of collagen; inflammation, vasoconstriction and secretion of growth factors develop in parallel. Disorders of collagen formation and the immune system are interrelated at the subcellular and molecular levels. These facts emphasize the relevance of the study of prooxidant and antioxidant systems in localized scleroderma.