ArticleAtherosclerosis2009
Influence of aspirin on SR-BI expression in human carotid plaques.
Article in Atherosclerosis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Potential Effects of Aspirin on Transcription Factors Related to the Inflammation in Atherosclerosis: A Systematic Review.Health science reports · 2026Review
- The potential role of scavenger receptor B type I (SR-BI) in SARS-CoV-2 infection.Immunity, inflammation and disease · 2023Review
- Rapid Regression of Carotid Artery Stenosis Shortly after Intensive Medical Therapy.Tomography (Ann Arbor, Mich.) · 2022Article
- Impact of coexisting coronary artery disease on the occurrence of cerebral ischemic lesions after carotid stenting.PloS one · 2014Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe recently showed that aspirin promotes scavenger receptor class-B type I (SR-BI) protein expression in vitro in primary human macrophages and in vivo in resident peritoneal macrophages of mice.
methodsWe compared SR-BI and CD68 expression in carotid atherosclerotic specimens from endarterectomized patients with (n=38) or without (n=19) low-dose aspirin medication (100 mg/day) prior to endarterectomy.
resultsWe found no differences concerning expression of CD68, indicating that aspirin did not influence macrophage content within atherosclerotic plaques. However, aspirin increased the expression of SR-BI protein in the analyzed specimens. In human THP-1-derived macrophages, induction of SR-BI protein by aspirin was abrogated by concomitant pharmacological inhibition of nuclear factor-kappa B (NF-kappaB). In in vitro experiments employing cultured primary macrophages from NF-kappaB/p50 KO mice, aspirin was not able to influence SR-BI expression. Additionally, no considerable effects on SR-BI expression were observed in vivo in resident macrophages of NF-kappaB/p50 KO mice orally treated with low or high doses of aspirin, respectively.
conclusionsWe suggest that aspirin treatment might lead to enhanced expression of SR-BI in human plaque macrophages and that this effect is dependent on the presence of NF-kappaB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.