title: Chemokines and cardiovascular risk.
abstract: Based on the importance of inflammation in atherogenesis, recent work has focused on whether plasma markers of inflammation can noninvasively diagnose and prognosticate atherosclerotic disorders. Although several studies support an important pathogenic role of chemokines in atherosclerosis, potentially representing attractive therapeutic targets in atherosclerotic disorders, this does not necessarily mean that chemokines are suitable parameters for risk prediction. In fact, the ability to reflect upstream inflammatory activity, stable levels in individuals, and high stability of the actual protein (eg, long half-life and negligible circadian variation) are additional important criteria for an ideal biomarker in cardiovascular disease. Although plasma/serum levels of certain chemokines (eg, interleukin- 8/CXCL8 and monocyte chemoattractant protein-1/CCL2) have shown to be predictive for future cardiac events in some studies, their role as clinical biomarkers is unclear, and their ability to predict subclinical atherosclerosis has been disappointing. Further prospective studies, including a larger number of patients, are needed to make any firm conclusion. Based on the participation of several chemokines in atherogenesis, it is possible that in the future, combined measurements of multiple chemokines could reveal as a "signature of disease" that can serve as a highly accurate method to assess for the presence of atherosclerotic disease.
authors.affiliation: Section of Clinical Immunology and InfectiousDiseases, Research Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo, Norway. pal.aukrust@rikshospitalet.no
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
authors.forename: Bente
authors.initials: B
authors.lastname: Halvorsen
authors.forename: Arne
authors.initials: A
authors.lastname: Yndestad
authors.forename: Thor
authors.initials: T
authors.lastname: Ueland
authors.forename: Erik
authors.initials: E
authors.lastname: Øie
authors.forename: Kari
authors.initials: K
authors.lastname: Otterdal
authors.forename: Lars
authors.initials: L
authors.lastname: Gullestad
authors.forename: Jan K
authors.initials: JK
authors.lastname: Damås
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000150:complications / Q000276:immunology*; D015415:Biomarkers / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000276:immunology; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000209:etiology / Q000276:immunology; D023903:Coronary Restenosis / Q000209:etiology / Q000276:immunology; D018450:Disease Progression; D014644:Genetic Variation; D016027:Heart Transplantation / Q000009:adverse effects; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000276:immunology*; D018836:Inflammation Mediators / Q000378:metabolism; D011379:Prognosis; D015203:Reproducibility of Results; D018570:Risk Assessment; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D018946:Chemokine CCL5; D018925:Chemokines; D018836:Inflammation Mediators