ArticleCirculation research2014
CD36-dependent 7-ketocholesterol accumulation in macrophages mediates progression of atherosclerosis in response to chronic air pollution exposure.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 183 citations in OpenAlex.
- Cardiopulmonary and Immune Effects of Environmental Particulate Exposures.Physiology (Bethesda, Md.) · 2026Review
- Review
- Modeling the Exposome in Murine Cardiovascular Disease.JACC. Basic to translational science · 2026Review
- Impact of air pollution on exacerbations of respiratory and cardiovascular diseases for the intensivist: a narrative review.Intensive care medicine experimental · 2026Review
- CD4+ T Cell Activation and Peripheral Immune Cell Influx into the Brain Following Wildfire Smoke Exposure is Modulated by a Saturated Fat Diet.Research square · 2026Article
- Links between Air Pollution and Aortic Diseases: Current Evidence for Future Prevention and Treatment.International journal of medical sciences · 2026Review
- A comprehensive review/expert statement on environmental risk factors of cardiovascular disease.Cardiovascular research · 2025Review
- Itaconate alleviates cholesterol burden via ABCA1 stabilization and cholesterol efflux.Atherosclerosis · 2025Article
- The Role and Phagocytic Mechanisms of Alveolar Macrophages in Inflammatory Responses Induced by Diesel Exhaust Particles.Environmental science & technology · 2025Article
- Ambient Particulate Matter Exposure Impairs Gut Barrier Integrity and Disrupts Goblet Cell Function.Biomedicines · 2025Article
- Article
- Long-Term Nitrogen Dioxide Exposure as a Possible 5-Year Mortality Risk Factor in Diabetic Patients Treated Using Off-Pump Surgical Revascularization-A Retrospective Analysis.Medicina (Kaunas, Lithuania) · 2024Article
- Bibliometric analysis of global research on air pollution and cardiovascular diseases: 2012-2022.Heliyon · 2024Article
- Air Pollution in Cardio-Oncology and Unraveling the Environmental Nexus:JACC. CardioOncology · 2024Review
- Understanding the Cardiovascular and Metabolic Health Effects of Air Pollution in the Context of Cumulative Exposomic Impacts.Circulation research · 2024Review
- Phytol from3 Biotech · 2024Article
- An update on ox-LDL-inducing vascular smooth muscle cell-derived foam cells in atherosclerosis.Frontiers in cell and developmental biology · 2024Review
- Effect of air pollution on the global burden of cardiovascular diseases and forecasting future trends of the related metrics: a systematic analysis from the Global Burden of Disease Study 2021.Frontiers in medicine · 2024Article
- Sitosterol-rich3 Biotech · 2023Article
- Assessing the timing and the duration of exposure to air pollution on cardiometabolic biomarkers in patients suspected of coronary artery disease.Environmental research · 2023Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleAir pollution exposure has been shown to potentiate plaque progression in humans and animals. Our previous studies have suggested a role for oxidized lipids in mediating adverse vascular effect of air pollution. However, the types of oxidized lipids formed in response to air pollutants and how this occurs and their relevance to atherosclerosis are not fully understood.
objectiveTo investigate the mechanisms by which particulate matter <2.5 μm (PM2.5) induces progression of atherosclerosis. METHODS AND
resultsAtherosclerosis-prone ApoE(-/-) or LDLR(-/-) mice were exposed to filtered air or concentrated ambient PM2.5 using a versatile aerosol concentrator enrichment system for 6 months. PM2.5 increased 7-ketocholesterol (7-KCh), an oxidatively modified form of cholesterol, in plasma intermediate density lipoprotein/low-density lipoprotein fraction and in aortic plaque concomitant with progression of atherosclerosis and increased CD36 expression in plaque macrophages from PM2.5-exposed mice. Macrophages isolated from PM2.5-exposed mice displayed increased uptake of oxidized lipids without alterations in their efflux capacity. Consistent with these finding, CD36-positive macrophages displayed a heightened capacity for oxidized lipid uptake. Deficiency of CD36 on hematopoietic cells diminished the effect of air pollution on 7-KCh accumulation, foam cell formation, and atherosclerosis.
conclusionsOur results suggest a potential role for CD36-mediated abnormal accumulations of oxidized lipids, such as 7-KCh, in air pollution-induced atherosclerosis progression.
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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.