ArticleParticle and fibre toxicology2018
Lipophilic components of diesel exhaust particles induce pro-inflammatory responses in human endothelial cells through AhR dependent pathway(s).
Article in Particle and fibre toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Understanding the Mechanism of Cardiotoxicity Induced by Nanomaterials: A Comprehensive Review.Small science · 2025Review
- Non-polar components in PMFrontiers in genetics · 2025Article
- The effects of photochemical aging and interactions with secondary organic aerosols on cellular toxicity of combustion particles.Journal of aerosol science · 2025Article
- Impact of the environmental pollution on cardiovascular diseases: From epidemiological to molecular evidence.Heliyon · 2024Review
- Exposure to urban nanoparticles at low PM[Formula: see text] concentrations as a source of oxidative stress and inflammation.Scientific reports · 2023Article
- Role of different mechanisms in pro-inflammatory responses triggered by traffic-derived particulate matter in human bronchiolar epithelial cells.Particle and fibre toxicology · 2023Article
- Variation in pentose phosphate pathway-associated metabolism dictates cytotoxicity outcomes determined by tetrazolium reduction assays.Scientific reports · 2023Article
- Modulating AHR function offers exciting therapeutic potential in gut immunity and inflammation.Cell & bioscience · 2023Review
- Wildfire-related smoke inhalation worsens cardiovascular risk in sleep disrupted rats.Frontiers in environmental health · 2023Article
- Effects of organic chemicals from diesel exhaust particles on adipocytes differentiated from human mesenchymal stem cells.Basic & clinical pharmacology & toxicology · 2023Article
- Mechanistic Insights into the Impact of Air Pollution on Pneumococcal Pathogenesis and Transmission.American journal of respiratory and critical care medicine · 2022Review
- Saponin attenuates diesel exhaust particle (DEP)-induced MUC5AC expression and pro-inflammatory cytokine upregulation via TLR4/TRIF/NF-κB signaling pathway in airway epithelium and ovalbumin (OVA)-sensitized mice.Journal of ginseng research · 2022Article
- Aryl hydrocarbon receptor (AhR) reveals evidence of antagonistic pleiotropy in the regulation of the aging process.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- The pro-inflammatory effects of combined exposure to diesel exhaust particles and mineral particles in human bronchial epithelial cells.Particle and fibre toxicology · 2022Article
- Article
- Carbon monoxide and a change of heart.Redox biology · 2021Review
- Combined Toxicity of Metal Nanoparticles: Comparison of Individual and Mixture Particles Effect.Advances in experimental medicine and biology · 2021Article
- The critical role of endothelial function in fine particulate matter-induced atherosclerosis.Particle and fibre toxicology · 2020Review
- Potential role of polycyclic aromatic hydrocarbons in air pollution-induced non-malignant respiratory diseases.Respiratory research · 2020Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
backgroundExposure to traffic-derived particulate matter (PM), such as diesel exhaust particles (DEP), is a leading environmental cause of cardiovascular disease (CVD), and may contribute to endothelial dysfunction and development of atherosclerosis. It is still debated how DEP and other inhaled PM can contribute to CVD. However, organic chemicals (OC) adhered to the particle surface, are considered central to many of the biological effects. In the present study, we have explored the ability of OC from DEP to reach the endothelium and trigger pro-inflammatory reactions, a central step on the path to atherosclerosis.
resultsExposure-relevant concentrations of DEP (0.12 μg/cm
conclusionLipophilic and semi-lipophilic chemicals seemed to detach from DEP, translocate through alveolar epithelial cells and trigger pro-inflammatory reactions in endothelial cells at exposure-relevant concentrations. These effects appeared to be triggered by AhR agonists, and involve PAR-2 signaling.
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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.