Cardiovascular disease dependent on inflammatory accelerated atherosclerosis leads to
increased mortality in rheumatoid arthritis (RA). In addition to traditional, Framingham risk factors,
several immuno-inflammatory cells, mediators and molecules may link atherosclerosis to arthritis.
Among immune cells, primarily TH1 cells, as well as endothelial cells play a crucial role in synovial
and vascular inflammation. Various cell surface molecules, such as adhesion receptors, CD40-CD40
ligand or members of the RANK-RANK ligand-osteoprotegerin system, as well as soluble pro-inflammatory cytokines,
chemokines, autoantibodies and proteases have been implicated in RA and vascular damage. The early assessment of
atherosclerosis and early intervention would decrease cardiovascular risk in RA.
Keywords: Atherosclerosis, biologics, cardiovascular disease, chemokines, cytokines, DMARDs, endothelial cells, proteases,
RANK ligand, rheumatoid arthritis.
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