ArticleToxicological sciences : an official journal of the Society of Toxicology2013
CD36 mediates endothelial dysfunction downstream of circulating factors induced by O3 exposure.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Modeling vascular inflammation and atherogenicity after inhalation of ambient levels of ozone: exploratory lessons from transcriptomics.Inhalation toxicology · 2017Pooled it
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- 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
- Environmental modulators of vascular physiology and inflammation.Experimental physiology · 2026Review
- A comprehensive review/expert statement on environmental risk factors of cardiovascular disease.Cardiovascular research · 2025Review
- Ozone exposure and cardiovascular disease: A narrative review of epidemiology evidence and underlying mechanisms.Fundamental research · 2025Review
- Characterization of Mild Delayed Gestational Hypertension in Rats Following Ozone Exposure.Cardiovascular toxicology · 2024Article
- Impact of Wildfires on Cardiovascular Health.Circulation research · 2024Review
- Cigarette smoking and air pollution exposure and their effects on cardiovascular diseases.Frontiers in public health · 2023Review
- Indirect mediators of systemic health outcomes following nanoparticle inhalation exposure.Pharmacology & therapeutics · 2022Review
- Neuroinflammatory and Neurometabolomic Consequences From Inhaled Wildfire Smoke-Derived Particulate Matter in the Western United States.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Integrative analysis reveals mouse strain-dependent responses to acute ozone exposure associated with airway macrophage transcriptional activity.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Physical Activity in Polluted Air-Net Benefit or Harm to Cardiovascular Health? A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2021Review
- Serum Albumin in Health and Disease: Esterase, Antioxidant, Transporting and Signaling Properties.International journal of molecular sciences · 2021Review
- Pulmonary delivery of the broad-spectrum matrix metalloproteinase inhibitor marimastat diminishes multiwalled carbon nanotube-induced circulating bioactivity without reducing pulmonary inflammation.Particle and fibre toxicology · 2021Article
- Short-term exposure to air pollution and biomarkers of cardiovascular effect: A repeated measures study.Environmental pollution (Barking, Essex : 1987) · 2021Article
- Fine particulate matter (PMAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Ambient air pollution exposure and radiographic pulmonary vascular volumes.Environmental epidemiology (Philadelphia, Pa.) · 2021Article
- Novel Mechanisms of Ozone-Induced Pulmonary Inflammation and Resolution, and the Potential Protective Role of Scavenger Receptor BI.Research report (Health Effects Institute) · 2021Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Inhaled pollutants induce the release of vasoactive factors into the systemic circulation, but little information is available regarding the nature of these factors or their receptors. The pattern recognition receptor CD36 interacts with many damage-related circulating molecules, leading to activation of endothelial cells and promoting vascular inflammation; therefore, we hypothesized that CD36 plays a pivotal role in mediating cross talk between inhaled ozone (O3)-induced circulating factors and systemic vascular dysfunction. O3 exposure (1 ppm × 4h) induced lung inflammation in wild-type (WT) mice, which was absent in the CD36 deficient (CD36(-/-)) mice. Acetylcholine (ACh)-evoked vasorelaxation was impaired in isolated aortas from O3-exposed WT mice but not in vessels from CD36(-/-) mice. To delineate whether vascular impairments were caused by lung inflammation or CD36-mediated generation of circulating factors, naïve aortas were treated with diluted serum from control or O3-exposed WT mice, which recapitulated the impairments of vasorelaxation observed after inhalation exposures. Aortas from CD36(-/-) mice were insensitive to the effects of O3-induced circulating factors, with robust vasorelaxation responses in the presence of serum from O3-exposed WT mice. Lung inflammation was not a requirement for production of circulating vasoactive factors, as serum from O3-exposed CD36(-/-) mice could inhibit vasorelaxation in naïve WT aortas. These results suggest that O3 inhalation induces the release of circulating bioactive factors capable of impairing vasorelaxation to ACh via a CD36-dependent signaling mechanism. Although lung inflammatory and systemic vascular effects were both dependent on CD36, the presence of circulating factors appears to be independent of CD36 and inflammatory responses.
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