ArticleArteriosclerosis, thrombosis, and vascular biology2019
Diesel Exhaust Induces Mitochondrial Dysfunction, Hyperlipidemia, and Liver Steatosis.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 51 citations in OpenAlex.
- Air Pollution Triggers Metabolomic Signature of Mitochondrial Dysfunction in Mice and Humans: Implications for Cardiovascular Disease Development.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Article
- Study on the Effect of Koumiss Extract in Alleviating Non-Alcoholic Fatty Liver Disease in Zebrafish Model by Improving Mitochondrial Function and Inhibiting Fat Deposition.Food science & nutrition · 2026Article
- Long-term exposure to air pollution and metabolites in children and young adults in a Swedish birth cohort.Journal of exposure science & environmental epidemiology · 2026Article
- 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
- Ultrafine particulate matter exposure induces gut microbiota dysbiosis together with ER stress in the liver and worsened atherosclerosis.Environment international · 2026Article
- Insights into the causal role of diesel exhaust particles in ventricular arrhythmogenesis: protective effects of antioxidant cerium oxide nanoparticles.Particle and fibre toxicology · 2025Article
- Diesel exhaust induces gut microbiome dysbiosis and reduced fecal acetate: Role of acetate supplementation.Ecotoxicology and environmental safety · 2025Article
- Integrated hepatic transcriptomics and metabolomics identify Pck1 as a key factor in the broad dysregulation induced by vehicle pollutants.Particle and fibre toxicology · 2024Article
- Diesel exhaust particle extract elicits an oxPAPC-like transcriptomic profile in macrophages across multiple mouse strains.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Review
- Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age.Toxics · 2024Article
- From Development to Place in Therapy of Lorlatinib for the Treatment of ALK and ROS1 Rearranged Non-Small Cell Lung Cancer (NSCLC).Diagnostics (Basel, Switzerland) · 2023Review
- APOE Peripheral and Brain Impact: APOE4 Carriers Accelerate Their Alzheimer Continuum and Have a High Risk of Suicide in PMBiomolecules · 2023Review
- Lung versus gut exposure to air pollution particles differentially affect metabolic health in mice.Particle and fibre toxicology · 2023Article
- Association between diesel exhaust exposure and mitochondrial DNA methylation.Carcinogenesis · 2022Article
- Silibinin Suppresses the Hyperlipidemic Effects of the ALK-Tyrosine Kinase Inhibitor Lorlatinib in Hepatic Cells.International journal of molecular sciences · 2022Article
- Atherosclerosis: Recent developments.Cell · 2022Review
- Obesity II: Establishing causal links between chemical exposures and obesity.Biochemical pharmacology · 2022Review
- Mitochondrial Dysfunction in Arsenic-Induced Hepatotoxicity: Pathogenic and Therapeutic Implications.Biological trace element research · 2022Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveAir pollution is associated with increased cardiovascular morbidity and mortality, as well as dyslipidemia and metabolic syndrome. Our goal was to dissect the mechanisms involved. Approach and Results: We assessed the effects of exposure to air pollution on lipid metabolism in mice through assessment of plasma lipids and lipoproteins, oxidized fatty acids 9-HODE (9-hydroxyoctadecadienoic) and 13-HODE (13-hydroxyoctadecadienoic), lipid, and carbohydrate metabolism. Findings were corroborated, and mechanisms were further assessed in HepG2 hepatocytes in culture. ApoE knockout mice exposed to inhaled diesel exhaust (DE, 6 h/d, 5 days/wk for 16 weeks) exhibited elevated plasma cholesterol and triglyceride levels, increased hepatic triglyceride content, and higher hepatic levels of 9-HODE and 13-HODE, as compared to control mice exposed to filtered air. A direct effect of DE exposure on hepatocytes was demonstrated by treatment of HepG2 cells with a methanol extract of DE particles followed by loading with oleic acid. As observed in vivo, this led to increased triglyceride content and significant downregulation of ACAD9 mRNA expression. Treatment of HepG2 cells with DE particles and oleic acid did not alter de novo lipogenesis but inhibited total, mitochondrial, and ATP-linked oxygen consumption rate, indicative of mitochondrial dysfunction. Treatment of isolated mitochondria, prepared from mouse liver, with DE particles and oleic acid also inhibited mitochondrial complex activity and β-oxidation.
conclusionsDE exposure leads to dyslipidemia and liver steatosis in ApoE knockout mice, likely due to mitochondrial dysfunction and decreased lipid catabolism.
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Registered trials
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