The DOI matches its Crossref record; 240 of the 240 references it cites were found in a registry or an index.
The Response-to-Retention Hypothesis of Early Atherogenesis
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“The retention of lipoproteins in the arterial extracellular matrix is a critical step in atherogenesis in which lipoproteins with higher affinity for arterial proteoglycans are more atherogenic (55, 56).”
From Role of the N- and C-Terminal Domains in Binding of Apolipoprotein E Isoforms to Heparan Sulfate and Dermatan Sulfate: A Surface Plasmon Resonance Study (2008) · cites this paper as [55]
In the citing paper
“The ECM has a central role in initiation of atherosclerosis, primarily through the interaction between the negatively charged side chains of proteoglycans (particularly chondroitin sulphate of biglycan and versican and heparin sulphate of perlecan 110 ) with positively charged apolipoproteins (especially apolipoprotein B) , which leads to the retention of plasma-derived lipoproteins 101,111 - as”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [113]
In the citing paper
“the interaction of apoB-containing lipoproteins (the non-HDL lipoproteins) with intimal extracellular proteoglycans (referred to as retention)1,43,44 inhibits the movement of the lipoproteins, thereby resulting in much higher subendothelial concentrations of these lipoproteins in the intima than in any other tissue45.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [1]
In the citing paper
“Atherosclerosis is a disease characterized by low-grade, chronic inflammation of the arterial wall and is triggered by the subendothelial retention of plasma-derived, apolipoprotein B (apoB)-containing lipoproteins in the affected inner layer of the arterial wall, the intima1–3.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [1]
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Cited by
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Macrophages in the Pathogenesis of Atherosclerosis
Moore, K. J., & Tabas, I. (2011) · Cell · doi:10.1016/j.cell.2011.04.005 · Cited by 2,669
Self-citationBorén, J., Chapman, M. J., Krauss, R. M., Packard, C. J., Bentzon, J. F., Binder, C. J., Daemen, M. J., Demer, L. L., Hegele, R. A., Nicholls, S. J., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz962 · Cited by 1,601
Tabas, I., Williams, K. J., & Borén, J. (2007) · Circulation · doi:10.1161/circulationaha.106.676890 · Cited by 1,399
Self-citationInflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities
Bäck, M., Yurdagul, A., Tabas, I., Öörni, K., & Kovanen, P. T. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0169-2 · Cited by 1,341
Self-citationChapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr112 · Cited by 1,227
Metadata
- Authors
- Williams, K. J., & Tabas, I.
- Affiliations
- Thomas Jefferson University (US)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 1995-05
- Volume
- 15
- Issue
- 5
- Pages
- 551-561
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC2924812
- OpenAlex
- W1968171440
- Cited by
- 1,413
- References
- 240
- Citations by year
- 2026: 27 · 2025: 34 · 2024: 37 · 2023: 40 · 2022: 42 · 2021: 39 · 2020: 55 · 2019: 47 · 2018: 42 · 2017: 41 · 2016: 59 · 2015: 73 · 2014: 60 · 2013: 56 · 2012: 60
- FWCI
- 12.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association
- National Institutes of Health (5p50hl021006-17, 5r01hl039703-08)
- Genentech
- National Heart, Lung, and Blood Institute (HL 38956, HL-39703, HL 21006, R01HL038956)
- 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 initiation, plaque retention, endothelial dysfunction
- MeSH terms
- Animals, Arteries, Arteriosclerosis, Humans, Lipoproteins, LDL, Models, Biological, Proteoglycans
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