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Recent insights into the cellular biology of atherosclerosis
Open accessAbstract
Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries at regions of disturbed blood flow and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein retention. Over time, this process stimulates a nonresolving inflammatory response that can cause intimal destruction, arterial thrombosis, and end-organ ischemia. Recent advances highlight important cell biological atherogenic processes, including mechanotransduction and inflammatory processes in endothelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switching of lesional smooth muscle cells. These advances illustrate how in-depth mechanistic knowledge of the cellular pathobiology of atherosclerosis can lead to new ideas for therapy.
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“Adding growth factors such as VEGF and PDGF to PLCL vascular scaffolds can effectively promote vascular endothelialization, accelerate migration and aggregation of endothelial cells and smooth muscle cells, and promote vascular regeneration and reconstruction [161].”
From Application of PLCL as a biodegradable polymer in biomedical engineering (2026) · cites this paper as [161]
Experimental — accuracy not yet measuredIn the citing paper
“Atherosclerosis is an age‐associated vascular disease characterised by the formation of plaques in arterial vessels, which can lead to the development of various cardiovascular disorders including myocardial infarction, stroke and sudden cardiac death (Tabas et al, 2015).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Tabas et al, 2015
In the citing paper
“Hypercholesterolemia, defined by elevated plasma low‐density lipoprotein (LDL) cholesterol, is a well‐established risk factor not only for cardiovascular disease (Borén et al. 2022; Steinberg 2013; Tabas et al. 2015; Boffa and Koschinsky 2019), but also for cognitive decline and dementia in later life (Kivipelto et al. 2001; Kivipelto and Solomon 2006; Livingston et al. 2024; Sparks et al. 2000, 2”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Tabas et al. 2015
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“[21] Tabas I, García-Cardeña G, Owens GK.”
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“These monocytes uptake excessive lipid to drive early plaque formation (Tabas et al., 2015).”
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“Key events in the atherosclerotic pathophysiology are (1) dyslipidemia-associated lipoprotein retention in the subintimal space of particular anatomical regions of the arterial tree, (2) physicochemical modifications of lipoproteins leading to endothelial dysfunction and activation, recruitment of leukocytes, and the…”
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Human Lipoproteins at Model Cell Membranes: Effect of Lipoprotein Class on Lipid Exchange
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“Modified LDL serves as the primary source of cholesterol accumulation and chronic inflammation in atherosclerotic plaques (Tabas et al., 2015).”
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Metadata
- Authors
- Tabas, I., García-Cardeña, G., & Owens, G. K.
- Affiliations
- Columbia University Irving Medical Center (US)
- Program in Human Biology and Translational Medicine, Harvard Medical School, Boston, MA 02115 4
- University of Virginia (US)
- Corresponding author
- Tabas, Ira
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2015-04-13
- Volume
- 209
- Issue
- 1
- Pages
- 13-22
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC4395483
- OpenAlex
- W1949072443
- Cited by
- 1,016
- References
- 107
- Citations by year
- 2026: 45 · 2025: 68 · 2024: 70 · 2023: 96 · 2022: 107 · 2021: 94 · 2020: 96 · 2019: 124 · 2018: 108 · 2017: 103 · 2016: 78 · 2015: 23
- FWCI
- 9.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Cell Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- National Institute on Aging (AG032443, R01AG032443)
- National Heart, Lung, and Blood Institute (R44HL118826, HL057353, HL087867, HL107497, HL075662, HL121008, HL118826, R01HL087867, R01HL057353, R01HL075662, R37HL057353, R01HL121008, R01HL107497, R41HL118826)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- atherosclerosis, endothelial dysfunction, disturbed blood flow, nonresolving inflammation, arterial thrombosis, end-organ ischemia, mechanotransduction, endothelial inflammation, macrophage origin, smooth muscle cell phenotypic switching, atherosclerosis treatment
- MeSH terms
- Animals, Endothelium, Vascular, Humans, Macrophages, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Mechanotransduction, Cellular, Endothelial Cells, Atherosclerosis
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