Oxidative stress in the pathology and treatment of systemic lupus erythematosus

Oxidative stress—generated through multiple mechanisms in a cell-type-specific manner—is a substantial contributor to disease pathogenesis, organ damage and comorbidities in patients with systemic lupus erythematosus (SLE)Pathways of oxidative pathogenesis, such as oxidative modification of self antigens and T-cell dysfunction, have been identifiedOrgan systems in which the clinical importance of oxidative damage in SLE has been recognized include the cardiovascular and renal systems and the skinBiomarkers of oxidative stress correlate directly with disease activity in SLEDepletion of glutathione (reflecting oxidative stress) might have a pathogenic role; its reversal by N-acetylcysteine seems to have therapeutic benefit in mouse models and patients with SLE