Abstract:
Systemic lupus erythematosus (SLE) is a systemic autoimmune rheumatic disease of unknown etiology with an ambiguous course and prognosis, developing on the basis of a genetically determined defect in immunoregulatory mechanisms, leading to overproduction of a wide range of organ-specific autoantibodies to various components of the nucleus and immune complexes that cause damage to tissues and immune-inflammatory disorders functions of internal organs. Pathology of the cardiovascular system, kidneys and central nervous system in SLE is one of the most frequent manifestations of the disease and largely determines its prognosis, and the pathogenetic structures of lesions of the myocardium, coronary, renal and cerebral vessels remain insufficiently studied. SLE is characterized by the development of vasculitis of varying severity. Activation of pro-inflammatory mediators, monocytes, T cells leads to endothelial damage. In recent years, the contribution of endothelial dysfunction (ED) (due to chronic inflammation) to the progression of systemic lupus erythematosus has been discussed.
