Mechanisms of inflammatory atherosclerosis in rheumatoid arthritis

Z. Szekanecz, G. Kerekes, Zsofia Kardos, Zsuzsa Barath, Laszlo Tamasi

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)35-46
Number of pages12
JournalCurrent Immunology Reviews
Volume12
Issue number1
Publication statusPublished - Apr 1 2016

Keywords

  • Atherosclerosis
  • Biologics
  • Cardiovascular disease
  • Chemokines
  • Cytokines
  • DMARDs
  • Endothelial cells
  • Proteases
  • RANK ligand
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

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