ArticleBasic research in cardiology2016
Acute exposure to air pollution particulate matter aggravates experimental myocardial infarction in mice by potentiating cytokine secretion from lung macrophages.
Article in Basic research in cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 77 citations in OpenAlex.
- Extreme Weather Events, Air Pollution, and Cardiovascular Health: Mechanisms and Challenges.Reviews in cardiovascular medicine · 2026Review
- Targeting the heart-immune axis after myocardial infarction: from inflammation to immunomodulation.Frontiers in cardiovascular medicine · 2026Review
- Insights into the causal role of diesel exhaust particles in ventricular arrhythmogenesis: protective effects of antioxidant cerium oxide nanoparticles.Particle and fibre toxicology · 2025Article
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
- A comprehensive review/expert statement on environmental risk factors of cardiovascular disease.Cardiovascular research · 2025Review
- Particulate matter air pollution: effects on the respiratory system.The Journal of clinical investigation · 2025Review
- The Role and Phagocytic Mechanisms of Alveolar Macrophages in Inflammatory Responses Induced by Diesel Exhaust Particles.Environmental science & technology · 2025Article
- Hypercholesterolemia, oxidative stress, and low-grade inflammation: a potentially dangerous scenario to blood-brain barrier.Metabolic brain disease · 2025Review
- Air Pollution and Myocardial Infarction-A New Smoker's Paradox?Journal of clinical medicine · 2024Article
- Hemolytic Properties of Fine Particulate Matter (PMToxics · 2024Article
- Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PMEnvironmental pollution (Barking, Essex : 1987) · 2024Article
- Toxicological Effects of Fine Particulate Matter (PMWater, air, and soil pollution · 2023Review
- CARD9 deficiency improves the recovery of limb ischemia in mice with ambient fine particulate matter exposure.Frontiers in cardiovascular medicine · 2023Article
- The macrophage senescence hypothesis: the role of poor heat shock response in pulmonary inflammation and endothelial dysfunction following chronic exposure to air pollution.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Environmental Stressors and the PINE Network: Can Physical Environmental Stressors Drive Long-Term Physical and Mental Health Risks?International journal of environmental research and public health · 2022Review
- Ambient Air Pollution and Risk for Stroke Hospitalization: Impact on Susceptible Groups.Toxics · 2022Article
- White and brown adipose tissue functionality is impaired by fine particulate matter (PMJournal of molecular medicine (Berlin, Germany) · 2022Review
- Influence of air pollutants on circulating inflammatory cells and microRNA expression in acute myocardial infarction.Scientific reports · 2022Article
- HSP70 as a biomarker of the thin threshold between benefit and injury due to physical exercise when exposed to air pollution.Cell stress & chaperones · 2021Review
- Fine particulate matter constituents associated with emergency room visits for pediatric asthma: a time-stratified case-crossover study in an urban area.BMC public health · 2021Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical, but not experimental evidence has suggested that air pollution particulate matter (PM) aggravates myocardial infarction (MI). Here, we aimed to describe mechanisms and consequences of PM exposure in an experimental model of MI. C57BL/6J mice were challenged with a PM surrogate (Residual Oil Fly Ash, ROFA) by intranasal installation before MI was induced by permanent ligation of the left anterior descending coronary artery. Histological analysis of the myocardium 7 days after MI demonstrated an increase in infarct area and enhanced inflammatory cell recruitment in ROFA-exposed mice. Mechanistically, ROFA exposure increased the levels of the circulating pro-inflammatory cytokines TNF-α, IL-6, and MCP-1, activated myeloid and endothelial cells, and enhanced leukocyte recruitment to the peritoneal cavity and the vascular endothelium. Notably, these effects on endothelial cells and circulating leukocytes could be reversed by neutralizing anti-TNF-α treatment. We identified alveolar macrophages as the primary source of elevated cytokine production after PM exposure. Accordingly, in vivo depletion of alveolar macrophages by intranasal clodronate attenuated inflammation and cell recruitment to infarcted tissue of ROFA-exposed mice. Taken together, our data demonstrate that exposure to environmental PM induces the release of inflammatory cytokines from alveolar macrophages which directly worsens the course of MI in mice. These findings uncover a novel link between air pollution PM exposure and inflammatory pathways, highlighting the importance of environmental factors in cardiovascular disease.
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