ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS
PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β
Article in Journal of the renin-angiotensin-aldosterone system : JRAAS. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Association between particulate matter air pollution and subclinical myocardial fibrosis in structurally normal hearts: a CMR-based study.European heart journal. Cardiovascular Imaging · 2026Article
- The role of different types of programmed cell death in myocardial fibrosis: from mechanisms to therapeutics.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
- Association between Long-term Exposure to Ambient Air Pollution and Myocardial Fibrosis Assessed with Cardiac MRI.Radiology · 2025Article
- Epigallocatechin-3-Gallate Inhibits Atrial Fibrosis and Reduces the Occurrence and Maintenance of Atrial Fibrillation and its Possible Mechanisms.Cardiovascular drugs and therapy · 2024Article
- Environmental Exposome and Atrial Fibrillation: Emerging Evidence and Future Directions.Circulation research · 2024Review
- Disruption of Atrial Rhythmicity by the Air Pollutant 1,2-Naphthoquinone: Role of Beta-Adrenergic and Sensory Receptors.Biomolecules · 2023Article
- Fine Particulate Matter Exposure Levels in Patients with Normal-Tension Glaucoma and Primary Open-Angle Glaucoma: A Population-Based Study from Taiwan.International journal of environmental research and public health · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectsTo discuss the influence of PM2.5 on myocardial fibrosis and related mechanism.
methodsPM2.5 particles were prepared into different concentrations of solution to drip into the mice's trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β
resultsThe higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β
conclusion1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β
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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.