CRP as a Mediator of Disease
Open Access
- 1 June 2004
- journal article
- review article
- Published by Ovid Technologies (Wolters Kluwer Health) in Circulation
- Vol. 109 (21_suppl_1), II-11-II-14
- https://doi.org/10.1161/01.cir.0000129507.12719.80
Abstract
Of the various hypotheses offered to explain atherosclerosis, inflammation now appears to provide a key to this pathological process. Inflammation has been shown to play a major role in precipitating a cascade of events from formation of the atheromatous lesion in response to vascular injury through lipid ingestion by macrophages, to subsequent rupture of the lesion, and myocardial infarction. Atherosclerosis shares many inflammatory features with rheumatoid arthritis (RA), an autoimmune disease, and drugs that block the inflammatory cytokine pathway now provide effective treatment for RA. In animal models, blockers of the inflammatory cytokine pathway appear to block mononuclear cell binding to arterial plaque. C-reactive protein (CRP), an inflammatory marker, may also play a proinflammatory role in activating monocyte chemotactic protein. Antiatherosclerotic drugs may be exerting some of their beneficial effects by inhibiting the harmful effects of CRP.This publication has 4 references indexed in Scilit:
- Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular EventsThe New England Journal of Medicine, 2002
- Acute-Phase Proteins and Other Systemic Responses to InflammationThe New England Journal of Medicine, 1999
- Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy MenThe New England Journal of Medicine, 1997
- The Prognostic Value of C-Reactive Protein and Serum Amyloid A Protein in Severe Unstable AnginaThe New England Journal of Medicine, 1994