Rheumatoid arthritis (RA), a prototypical immune-mediated inflammatory disease, is characterized by increased cardiovascular morbidity and mortality, independent from the established cardiovascular risk factors. The chronic inflammatory state, a hallmark of RA, is considered to be a driving force for accelerated atherogenesis. Concurrent conditions that expedite the atherosclerotic process in RA involve endothelial dysfunction, dyslipidemia and procoagulant changes. These facilitating states can be reversed by retraction of the systemic inflammatory activity. Consequently, aggressive control of disease activity has been suggested to be instrumental for cardiovascular risk reduction. In the present review, we focus on these critical determinant that promote premature atherosclerosis in RA.
Keywords: Atheroslerosis, rheumatoid arthritis, cardiovascular risk factors, chronic inflammation, human cancers, pathogenesis, skin carcinogenesis, hydroxytyrosol, tyrosol, Hydroxytyrosol (3,4 DHPEA-EDA), HL60 (human promyelocytic leukemia cells), caspases, poly-ADP-ribose polym-erase, cytochrome, cytosolic proteins, Her-2/neu, Her2/neu on-cogene, cellular proliferation, transformation, differentiation, mo-tility, metastasis, p185 Her-2/neu oncoprotein, BT-474, SK-Br3 cells, trastuzumab (Her-ceptinTM), Akt, PI-3 kinase/Akt pathway, erythrodiol, pentacyclic triterpenic acids, Olea Euopaea, HT-29 cells, reactive oxygen species, Confocal micros-copy analysis, squalene, cholesterol biosynthesis, Ras farnesylation, MAPK pathway, Bcl-2 pathways, Apaf 1, apoptosome, necrotic cells, Caiazzana and Ravece, colorectal can-cer cell lines, ATM-p53, pinoresinol, oleocanthal, Bcl-2 family, Bax, trol of the G2/M checkpoint, p53 is directly controlled by the ATM-ATR genes
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