Systemic lupus erythematosus and glycation process

Systemic lupus erythematosus (SLE) is a disease of unclear causes, which leads to major immunological disorders. It is characterized by an abnormal immune system activity resulting in the production of autoantibodies. In patients, antibodies targeting normal nuclear components, double-stranded DNA (dsDNA), and phospholipids (cardiolipin) can be detected. The inflammatory process occurs in various tissues and organs, damaging their functions and structure. Disease’s course includes stages of acute symptoms and remissions, and there is no known cure. Pathogenesis and biochemical pathways accompanying systemic lupus erythematosus are widely studied, as existing medication can only bring temporary relief to patients. The recent findings suggest that occurrence of SLE depends on interactions between genetic background of the disease and environmental risk factors such as exposure to tobacco smoke, chemical factors, and hormonal therapy. In the addition, chronic inflammation accompanying SLE disturbs oxidative/antioxidative balance. These processes are linked to intensified advanced glycation end products (AGEs) formation, thus level of AGEs themselves and their receptors (RAGE, sRAGE) are gaining researches attention.