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Inflammation in Atherosclerosis: From Vascular Biology to Biomarker Discovery and Risk Prediction
Abstract
Recent investigations of atherosclerosis have focused on inflammation, providing new insight into mechanisms of disease. Inflammatory cytokines involved in vascular inflammation stimulate the generation of endothelial adhesion molecules, proteases, and other mediators, which may enter the circulation in soluble form. These primary cytokines also induce production of the messenger cytokine interleukin-6, which stimulates the liver to increase production of acute-phase reactants such as C-reactive protein. In addition, platelets and adipose tissue can generate inflammatory mediators relevant to atherothrombosis. Despite the irreplaceable utility of plasma lipid profiles in assessment of atherosclerotic risk, these profiles provide an incomplete picture. Indeed, many cardiovascular events occur in individuals with plasma cholesterol concentrations below the National Cholesterol Education Program thresholds of 200 mg/dL for total cholesterol and 130 mg/dL for low-density lipoprotein (LDL) cholesterol. The concept of the involvement of inflammation in atherosclerosis has spurred the discovery and adoption of inflammatory biomarkers for cardiovascular risk prediction. C-reactive protein is currently the best validated inflammatory biomarker; in addition, soluble CD40 ligand, adiponectin, interleukin 18, and matrix metalloproteinase 9 may provide additional information for cardiovascular risk stratification and prediction. This review retraces the biology of atherothrombosis and the evidence supporting the role of inflammatory biomarkers in predicting primary cardiovascular events in this biologic context.
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“It has now become clear that low-grade chronic inflammation is a key player in the pathogenesis of most CNCDs.”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [6]
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Metadata
- Authors
- Packard, R. R. S., & Libby, P.
- Affiliations
- Leducq Center for Cardiovascular Research, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
- Brigham and Women's Hospital (US)
- Corresponding author
- Libby, Peter
- ORCID
- Libby, Peter
- Venue
- Clinical Chemistry
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-01-01
- Volume
- 54
- Issue
- 1
- Pages
- 24-38
- ISSN
- 0009-9147 (ISSN-L)
- 1530-8561
- OpenAlex
- W2023647145
- Cited by
- 925
- References
- 169
- Citations by year
- 2026: 10 · 2025: 18 · 2024: 10 · 2023: 20 · 2022: 19 · 2021: 39 · 2020: 44 · 2019: 39 · 2018: 37 · 2017: 39 · 2016: 61 · 2015: 69 · 2014: 65 · 2013: 93 · 2012: 81
- FWCI
- 5.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Clinical Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- atherosclerosis, vascular inflammation, inflammatory markers, cardiovascular risk prediction, C-reactive protein, interleukin-6, atherothrombosis, platelets, adipose tissue, soluble CD40 ligand, adiponectin, IL-18, MMP-9, endothelial adhesion molecules, acute phase proteins, low LDL cholesterol
- MeSH terms
- Cardiovascular Diseases, Humans, Inflammation, Risk, Biomarkers, Inflammation Mediators, Atherosclerosis
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