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Critical Determinants of Cardiovascular Risk in Rheumatoid Arthritis

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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: ATM-p53; Akt; Apaf 1; Atheroslerosis; BT-474; Bax; Bcl-2 family; Bcl-2 pathways; Caiazzana and Ravece; Confocal micros-copy analysis; HL60 (human promyelocytic leukemia cells); HT-29 cells; Her-2/neu; Her2/neu on-cogene; Hydroxytyrosol (3,4 DHPEA-EDA); MAPK pathway; Olea Euopaea; PI-3 kinase/Akt pathway; Ras farnesylation; SK-Br3 cells; apoptosome; cardiovascular risk factors; caspases; cellular proliferation; cholesterol biosynthesis; chronic inflammation; colorectal can-cer cell lines; cytochrome; cytosolic proteins; differentiation; erythrodiol; human cancers; hydroxytyrosol; metastasis; mo-tility; necrotic cells; oleocanthal; p185 Her-2/neu oncoprotein; pathogenesis; pentacyclic triterpenic acids; pinoresinol; poly-ADP-ribose polym-erase; reactive oxygen species; rheumatoid arthritis; skin carcinogenesis; squalene; transformation; trastuzumab (Her-ceptinTM); trol of the G2/M checkpoint, p53 is directly controlled by the ATM-ATR genes; tyrosol

Document Type: Research Article

Publication date: 01 January 2011

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