The arterial microenvironment: the where and why of atherosclerosis
Open accessAbstract
The formation of atherosclerotic plaques in the large and medium sized arteries is classically driven by systemic factors, such as elevated cholesterol and blood pressure. However, work over the past several decades has established that atherosclerotic plaque development involves a complex coordination of both systemic and local cues that ultimately determine where plaques form and how plaques progress. Although current therapeutics for atherosclerotic cardiovascular disease primarily target the systemic risk factors, a large array of studies suggest that the local microenvironment, including arterial mechanics, matrix remodelling and lipid deposition, plays a vital role in regulating the local susceptibility to plaque development through the regulation of vascular cell function. Additionally, these microenvironmental stimuli are capable of tuning other aspects of the microenvironment through collective adaptation. In this review, we will discuss the components of the arterial microenvironment, how these components cross-talk to shape the local microenvironment, and the effect of microenvironmental stimuli on vascular cell function during atherosclerotic plaque formation.
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Oxidative lipoprotein modifications generate oxidized phospholipids and other lipid mediators that can induce leukocyte recruitment and activation in the arterial intima.
“Oxidative lipoprotein modifications lead to the generation of oxidized phospholipids (oxPLs) and other lipid mediators that have the potential to influence inflammation and atherogenesis in the arterial intima by inducing leukocyte recruitment and leukocyte activation49,50.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [49]
In early atherosclerosis, apoB-containing lipoproteins retained in the subendothelial matrix of medium-to-large arteries stimulate a robust inflammatory response that includes chemotactic factors driving leukocyte recruitment.
“As discussed above, in early atherosclerosis, apoB-containing lipoproteins are retained in the subendothelial matrix of medium-to-large arteries and stimulate a robust inflammatory response, which includes the release of chemotactic factors that drive leukocyte recruitment49.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [49]
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References 187 · Cited by 185
- Authors
- Yurdagul, A., Finney, A. C., Woolard, M. D., & Orr, A. W.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2016-05-11
- Volume
- 473
- Issue
- 10
- Pages
- 1281-1295
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC5410666
- OpenAlex
- W2355649199
- Cited by
- 185
- References
- 187
- Citations by year
- 2026: 8 · 2025: 15 · 2024: 19 · 2023: 16 · 2022: 21 · 2021: 27 · 2020: 17 · 2019: 27 · 2018: 17 · 2017: 14 · 2016: 4
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Journal (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL098435)
- National Institute of General Medical Sciences (U54GM104940)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Physical Sciences › Engineering › Biomedical Engineering › Elasticity and Material Modeling
- Keywords
- atherosclerosis, atherosclerotic plaque formation, arterial wall mechanics, extracellular matrix remodeling, lipid accumulation, plaque progression
- MeSH terms
- Animals, Endothelium, Vascular, Humans, Models, Biological, Risk Factors, Atherosclerosis, Plaque, Atherosclerotic
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