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Key Points Oxidative stressgenerated through multiple mechanisms in a cell-type-specific manneris 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 identified Organ systems in which the clinical importance of oxidative damage in SLE has been recognized include the cardiovascular and renal systems and the skin Biomarkers of oxidative stress correlate directly with disease activity in SLE Depletion of glutathione (reflecting oxidative stress) might have a pathogenic role

Knockdown of preproglucagon expression in the hindbrain as well as central GLP-1R antagonism results in hyperphagia and body weight gain in rats indicating that these neurons are essential for maintenance of normal body weight (Barrera et al., 1996)

This pathway safely degrades homocysteinea potentially toxic byproduct of metabolisminto cysteine through two sequential enzymatic steps involving cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE)

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References 1.Meister A., Anderson M.E