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Mechanisms of Inflammatory Atherosclerosis in Rheumatoid Arthritis

[ Vol. 12 , Issue. 1 ]


Zoltan Szekanecz, Gyorgy Kerekes, Zsofia Kardos, Zsuzsa Barath and Laszlo Tamasi   Pages 35 - 46 ( 12 )


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.


Atherosclerosis, biologics, cardiovascular disease, chemokines, cytokines, DMARDs, endothelial cells, proteases, RANK ligand, rheumatoid arthritis.


Department of Rheumatology, Institute of Medicine, University of Debrecen, Faculty of Medicine Nagyerdei str 98, 4032, Debrecen, Hungary.

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