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 effectively promotes vascular endothelialization, accelerates migration and aggregation of endothelial cells and smooth muscle cells, and promotes vascular regeneration and reconstruction.
“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]
The SMC phenotypic-switching section discusses PDGF-BB as a regulator of cultured smooth muscle cells, while the endothelial mechanotransduction section discusses VEGFR2 in flow sensing. Neither section addresses adding VEGF or PDGF to PLCL scaffolds or the claimed effects on endothelialization, cell migration, and vascular reconstruction; searches for those terms found no supporting passage in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measuredAtherosclerosis is an age-associated vascular disease characterised by plaque formation in arterial vessels, which can lead to cardiovascular disorders.
“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
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- 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
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Physiology › 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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