The Biological Role of Inflammation in Atherosclerosis
Abstract
The concept of the involvement of inflammation in the pathogenesis of atherosclerosis has existed since the 1800s, stemming from sentinel pathologic observations made by Rudolf Virchow, Karl Rokitansky, and others. Our understanding of the complex role played by immune and inflammatory mediators in the initiation and progression of atherosclerosis has evolved considerably in the intervening years, and today, a dramatically evolved understanding of these processes has led to advances in both diagnostic and prognostic approaches, as well as novel treatment modalities targeting inflammatory and immune mediators. Therapeutic interventions working through multiple mechanisms involved in atheroma pathogenesis, such as statins, which both lower lipids and alter the inflammatory milieu in the vessel wall, hold promise for the future. In this brief review, we explore the biological role of inflammation in atherosclerosis, with a focus on cellular involvement in both acute and chronic inflammation, and outline novel biomarkers of inflammation and atherosclerosis with a particular focus on the potential application of these novel approaches in improving strategies for disease diagnosis and management.
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Atherosclerosis is the result of prolonged and excessive inflammatory processes in the vascular wall, often beginning with inflammatory changes in the endothelium and characterized by expression of adhesion molecules.
“Accumulating evidence indicates that AS is the result of a prolonged and excessive inflammatory processes in the vascular wall, which often begins with inflammatory changes in the endothelium and is characterized by the expression of adhesion molecules.2, 3”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [3]
Inflammation participates centrally in all stages of AS from initial lesion to end-stage thrombotic complications.
“Inflammation participates centrally in all stages of AS from the initial lesion to end‐stage thrombotic complications.”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [3]
The process of AS often begins with inflammatory changes in the endothelium, characterized by expression of adhesion molecules.
“The process often begins with inflammatory changes in the endothelium, characterized by expression of adhesion molecules.2, 3”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [3]
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References 108 · Cited by 168
- Authors
- Wong, B. W., Meredith, A., Lin, D., & McManus, B. M.
- Affiliations
- University of British Columbia (CA)
- Venue
- Canadian Journal of Cardiology
- Publisher
- Elsevier BV
- Published
- 2012-11
- Volume
- 28
- Issue
- 6
- Pages
- 631-641
- ISSN
- 0828-282X (ISSN-L)
- OpenAlex
- W2014610911
- Cited by
- 168
- References
- 108
- Citations by year
- 2025: 2 · 2024: 11 · 2023: 11 · 2022: 6 · 2021: 16 · 2020: 19 · 2019: 19 · 2018: 18 · 2017: 13 · 2016: 8 · 2015: 13 · 2014: 16 · 2013: 12 · 2012: 2
- FWCI
- 1.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Canadian Journal of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- inflammation, atherosclerosis, immune mediators, chronic inflammation, acute inflammation, inflammatory markers, statins, atherosclerosis diagnosis, anti-inflammatory therapy
- MeSH terms
- Animals, Chronic Disease, Humans, Immune System, Inflammation, Oxidative Stress, Disease Progression, Inflammation Mediators, Atherosclerosis
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