ArticleInhalation toxicology2011
Hypercholesterolemia potentiates aortic endothelial response to inhaled diesel exhaust.
Article in Inhalation toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- Association of oil spill-related volatile organic compound exposure with CVD-related biomarkers in the Gulf Long-term Follow-up Study.Annals of work exposures and health · 2026Article
- Links between Air Pollution and Aortic Diseases: Current Evidence for Future Prevention and Treatment.International journal of medical sciences · 2026Review
- Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution: Part 3 of a 3-Part Series.Journal of the American College of Cardiology · 2017Review
- Particulate matter and atherosclerosis: a bibliometric analysis of original research articles published in 1973-2014.BMC public health · 2016Review
- Epigenetic Regulation in Particulate Matter-Mediated Cardiopulmonary Toxicities: A Systems Biology Perspective.Current pharmacogenomics and personalized medicine · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundInhalation of diesel exhaust induces vascular effects including impaired endothelial function and increased atherosclerosis.
objectiveTo examine the in vivo effects of subchronic diesel exhaust exposure on endothelial cell transcriptional responses in the presence of hypercholesterolemia.
methodsApoE (-/-) and ApoE (+/+) mice inhaled diesel exhaust diluted to particulate matter levels of 300 or 1000 μg/m³ vs. filtered air. After 30 days, endothelial cells were harvested from dispersed aortic cells by fluorescent-activated cell sorting (FACS). Relative mRNA abundance was evaluated by microarray analysis to measure strain-specific transcriptional responses in mice exposed to dilute diesel exhaust vs. filtered air.
resultsForty-nine transcripts were significantly dysregulated by >2.8-fold in the endothelium of ApoE (-/-) mice receiving diesel exhaust at 300 or 1000 μg/m³. These included transcripts with roles in plasminogen activation, endothelial permeability, inflammation, genomic stability, and atherosclerosis; similar responses were not observed in ApoE (+/+) mice.
conclusionsThe potentiation of diesel exhaust-related endothelial gene regulation by hypercholesterolemia helps to explain air pollution-induced vascular effects in animals and humans. The observed regulated transcripts implicate pathways important in the acceleration of atherosclerosis by air pollution.
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Registered trials
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