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.
