Endothelium is now considered as a dynamic tissue that plays an active role in inflammation, immune response and coagulation. Pro-inflammatory cytokines, circulating autoantibodies and immune-complexes might interact with the endothelial cells inducing a pro-inflammatory and pro-coagulant phenotype. Moreover, the endothelium itself is able to synthesize growth factors, cytokines, chemokines and to express adhesion molecules that cooperate in recluting leukocytes locally. In addition, it has been shown that endothelial cells can express MHC class II molecules on the cell surface so acting as antigen presenting cells. In this regard it is not surprising that endothelial cells are strongly involved in pathogenic processes associated with systemic autoimmune vasculitides as well as with vasculopathies mediated by anti-phospholipid antibodies. Local inflammatory processes are now widely accepted to play a role in triggering the formation of the atherosclerotic plaque as well as to favour the plaque instability and rupture (athero-thrombosis). Recent epidemiological studies clearly reported an association between systemic autoimmune diseases (Systemic Lupus Erythematosus, Rheumatoid Arthritis) and accelerated atherosclerosis. Besides the well-known risk factors such as hypertension, dyslipidemia and steroid therapy, it has been suggested that mediators able to induce an activation/damage of the endothelium can also play a role in inducing the atherosclerotic plaque formation and its instability. The demonstration that statins counteract the endothelial activation mediated by autoantibodies or by cytokines in experimental models suggests the potential use of such a drug family in preventing the atherosclerosis in chronic inflammatory diseases.
|Translated title of the contribution||Thrombotic risk, endothelial disfunction and systemic autoimmune diseases|
|Number of pages||12|
|Journal||Progressi in Reumatologia|
|Publication status||Published - 2002|
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