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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
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“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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Citations
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“Besides promoting atherosclerosis, inflammation also plays a significant role in the process of plaque rupture and arterial thrombosis, leading to vascular occlusion and infarction [13].”
BackgroundmiR-146a deficiency in hematopoietic cells is not involved in the development of atherosclerosis
Monte-Monge, A. D., Arroyo, A. B., Andrés‐Manzano, M. J., García‐Barberá, N., Caleprico, M. S., Vicente, V., Roldán, V., Gónzález‐Conejero, R., Martı́nez, C., & Andrés, V. (2018) · PLoS ONE · doi:10.1371/journal.pone.0198932 · Cited by 18
Li, A. H., Sun, Y., Drummer, C., Lu, Y., Yu, D., Zhou, Y., Li, X., Pearson, S. J., Johnson, C., Yu, C. C., et al. (2019) · Frontiers in Physiology · doi:10.3389/fphys.2019.00433 · Cited by 18
“…the anti-inflammatory cytokines TGF-β, IL-4, and IL-10 from the database ArrayExpress (Braun et al., 2013; Teles et al., 2013; Bald et al., 2014; Jin et al., 2014; Kharma et al., 2014; Montoya et al., 2014; Polak et al., 2014, 2017; Duncan et al., 2015; Kolesnikov et al., 2015; Tan et al., 2015).”
BackgroundMaqbool, A., Watt, N. T., Haywood, N. J., Viswambharan, H., Skromna, A., Makava, N., Visnagri, A., Shawer, H. M., Bridge, K., Muminov, S., et al. (2020) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00389.2019 · Cited by 20
“This so called “oxidative stress” or “endothelial dysfunction” has a range of effects that could accelerate the development of vascular disease (2), principal among which is thought to be oxidative modification of circulating low-density lipoprotein (LDL), which leads to an adhesion molecule and inflammatory cell-medi…”
Murphy, P. A., Jailkhani, N., Nicholas, S.-A. E., Rosario, A. M. D., Balsbaugh, J. L., Begum, S., Kimble, A. L., & Hynes, R. O. (2020) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.120.314013 · Cited by 16
Crude leaf extracts of Piperaceae species downmodulate inflammatory responses by human monocytes
Finato, A. C., Fraga‐Silva, T. F. D. C., Prati, A. U. C., Souza, A. A., Mazzeu, B. F., Felippe, L. G., Pinto, R. A., Golim, M. D. A., de Arruda, M. S. P., Furlan, M., et al. (2018) · PLoS ONE · doi:10.1371/journal.pone.0198682 · Cited by 18
Gut Microbiota-Derived Metabolites and Cardiovascular Disease: Focus on Trimethylamine- N -oxide
He, M., Tan, C. P., & Liu, Y. (2025) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.5c08378 · Cited by 19
A novel therapeutic strategy for atherosclerosis: autophagy-dependent cholesterol efflux
Guo, H., Wei, D., Liu, R., Zhang, C., Jiang, S., Wang, W., Hu, H., Shen, L., & Liang, X. (2022) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-021-00870-5 · Cited by 17
“As the disease progresses, atherosclerotic plaques block the blood vessels, leading to progressive stenosis of the vascular lumen, which ultimately results in cardiovascular disease and peripheral vascular disease [81].”
BackgroundHou, X., Dai, H., & Zheng, Y. (2022) · Bioengineered · doi:10.1080/21655979.2022.2039467 · Cited by 17
“Atherosclerosis is a chronic progressive inflammatory disorder in which plaques form inside the arteries, and is the primary cause of morbidity and mortality in the world [1,2].”
BackgroundElectronic Cigarette and Atherosclerosis: A Comprehensive Literature Review of Latest Evidences
Damay, V. A., Setiawan, I., Lesmana, R., Akbar, M. R., Lukito, A. A., Tarawan, V. M., Martha, J. W., & Nugroho, J. (2022) · International Journal of Vascular Medicine · doi:10.1155/2022/4136811 · Cited by 17
“Inactive VSMC is contractile, expressing smooth muscle myosin heavy chain (MYH11) and smooth muscle actin alpha-2 (ACTA2) [21].”
BackgroundPrognostic value of plasma adipokine chemerin in patients with coronary artery disease
Wang, B., Kou, W., Ji, S., Shen, R., Ji, H., Zhuang, J., Zhao, Y., Li, B., Peng, W., Yu, X., et al. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.968349 · Cited by 17
“Atherogenic processes involve several kinds of cells, including the inflammation and mechanotransduction of endothelial cells (ECs), activation of lesion macrophages, and phenotypic switching of smooth muscle cells (SMCs) (18).”
BackgroundYadav, S. K., Das, S., Lincon, A., Saha, S., Dasgupta, S. B., Ray, S. K., & Das, S. (2024) · International Journal of Pharmaceutics · doi:10.1016/j.ijpharm.2023.123737 · Cited by 17
Sirca, T. B., Muresan, M. E., Pallag, A., Marian, E., Jurca, T., Vicaș, L. G., Blaj-Tunduc, I. P., Manole, F., & Ștefan, L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25052962 · Cited by 22
Liang, W., Wei, R., Zhu, X., Li, J., Lin, A., Chen, J., Wu, W., & Jie, Q. (2024) · Molecular Medicine · doi:10.1186/s10020-023-00753-z · Cited by 17
“…has documented the high plasma levels of low-density lipoprotein (LDL) as one of the most vital risk factors of AS, and LDL may accumulate in the sub-endothelial space of the arterial wall and subsequently forms oxidized LDL (oxLDL), which may trigger an inflammatory response (Tabas et al. 2015).”
BackgroundFrismantiene, A., Kyriakakis, E., Dasen, B., Erné, P., Resink, T. J., & Philippova, M. (2017) · Cell Adhesion & Migration · doi:10.1080/19336918.2017.1319545 · Cited by 17
“changes in cellular morphology in 2D, which is considered as a primary and classical hallmark of SMC phenotype switch.(1,7) Most of our knowledge on cell adhesion properties during SMC phenotype transition is derived from reductionist studies which investigated the functional properties of any given adhesion molecule…”
BackgroundBabaev, V. R., Ding, L., Zhang, Y., May, J. M., Ramsey, S. A., Vickers, K. C., & Linton, M. F. (2018) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.118.312206 · Cited by 17
Yang, K., Zeng, L., Ge, A., Pan, X., Bao, T., Long, Z., Tong, Q., Yuan, M., Zhu, X., Ge, J., et al. (2020) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.15979 · Cited by 16
Wojewoda, M., Tyrankiewicz, U., Gwóźdź, P., Skórka, T., Jablonska, M., Orzyłowska, A., Jasiński, K., Jasztal, A., Przyborowski, K., Kostogrys, R. B., et al. (2016) · Scientific Reports · doi:10.1038/srep24714 · Cited by 17
Effect of bilayer charge on lipoprotein lipid exchange
Browning, K. L., Lind, T. K., Maric, S., Barker, R. D., Cárdenas, M., & Malmsten, M. (2018) · Colloids and Surfaces B Biointerfaces · doi:10.1016/j.colsurfb.2018.01.043 · Cited by 17
“[2, 35] As a result of the latter, antioxidant treatment has been demonstrated to result in reduced atherosclerotic plaque formation in clinical trials.”
Lo, H., Ma, M., Shieh, J., Chen, H., & Wu, W. (2018) · International Journal of Nanomedicine · doi:10.2147/ijn.s156880 · Cited by 17
Conte, L., Somacal, S., Nichelle, S. M., Rampelotto, C., Robalo, S., Roehrs, M., & Emanuelli, T. (2019) · Journal of Nutrition and Metabolism · doi:10.1155/2019/9407069 · Cited by 15
“*e parallel release of proinflammatory cytokines, growing factors, and metalloproteinases by macrophages promotes cell recruitment, angiogenesis, apoptosis, and degradation of the extracellular matrix [2].”
BackgroundLiu, H., Li, X., Yan, G., & Lun, R. (2019) · RSC Advances · doi:10.1039/c9ra04726c · Cited by 16
Su, Q., Dong, X., Tang, C., Wei, X., Hao, Y., & Wu, J. (2021) · Open Medicine · doi:10.1515/med-2021-0209 · Cited by 16
“The etiology of AS is still unknown, but apoptosis and injury of endothelial cells caused by various factors are considered to be the main cause of AS [4,5].”
BackgroundNuclear Receptors and Clock Components in Cardiovascular Diseases
Pourcet, B., & Duez, H. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22189721 · Cited by 19
Belce, A., Özkan, B. N., Dumlu, F. S., Uzunoğlan, B. H. Ş., & Güler, E. M. (2022) · Clinical and Experimental Hypertension · doi:10.1080/10641963.2022.2036993 · Cited by 17
“Many cells and cytokines such as macrophages, T and B lymphocyte cells, dendritic cells, endothelial cells, vascular smooth muscle cells, ILs, adhesion molecules, and tumor necrosis factor (TNF-α) cause the formation of the atherosclerotic process (6).”
BackgroundHowe, K. L., Cybulsky, M. I., & Fish, J. E. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.888390 · Cited by 16
“In contrast to classic dogma citing loss of endothelial barrier integrity and passive movement of low-density lipoprotein (LDL) into the vessel wall (23, 24), transport of LDL cholesterol (a critical event in atherogenesis) requires active endothelial transcellular transport via expression of scavenger receptor class…”
BackgroundDing, R., Ren, X., Sun, Q., Sun, Z., & Duan, J. (2022) · Journal of Advanced Research · doi:10.1016/j.jare.2022.08.012 · Cited by 17
“The activation of inflammatory pathways is mainly involved in endothelial dysfunction, and atherosclerosis is thought to be accompanied by flowmediated inflammatory changes in endothelial cells (ECs) [107].”
Background
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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