Mechanisms of premature atherosclerosis in rheumatoid arthritis and lupus

Abstract

Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), the two most common systemic autoimmune disorders, have both unique and overlapping manifestations. One feature they share is a significantly enhanced risk of atherosclerotic cardiovascular (CV) disease that significantly contributes to morbidity and mortality. The primary mechanisms that drive CV damage in these diseases remain to be fully characterized, but recent discoveries indicate that distinct inflammatory pathways and immune dysregulation characteristic of RA and SLE likely play prominent roles. This review focuses on analyzing the major mechanisms and pathways potentially implicated in the acceleration of atherothrombosis and CV risk in SLE and RA, as well as in the identification of putative preventive strategies that may mitigate vascular complications in systemic autoimmunity.

Figure 1

An interplay between traditional cardiovascular risk factors and disease-specific traits leads to enhanced prevalence of atherosclerosis in rheumatoid arthritis and systemic lupus erythematosus. Abbreviations: TNF, tumor necrosis factor; IL, interleukin; IFN, interferon; LDG, low density granulocyte; piHDL, proinflammatory high density lipoprotein; oxLDL, oxidized low density lipoprotein; RF, rheumatoid factor; CCP, anti-cyclic citrullinated peptide; IC, immune complexs.