ArticleScientific reports2016
Phenanthrene exposure induces cardiac hypertrophy via reducing miR-133a expression by DNA methylation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 67 citations in OpenAlex.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Paternal sleep deprivation and cardiac dysfunction in offspring: A perspective of myocardial hypertrophy.Experimental physiology · 2026Article
- Roles of different methylation modifications in cardiovascular disease.Frontiers of medicine · 2025Review
- Review
- Therapeutic potential of miR-133a-transfected bone marrow mesenchymal stem cell transplantation in improving cardiac function post-myocardial infarction.Journal of cardiothoracic surgery · 2025Article
- Global Air Pollutant Phenanthrene and Arrhythmic Outcomes in a Mouse Model.Environmental health perspectives · 2023Article
- Article
- Relationship between miR-203a inhibition and oil-induced toxicity in early life stage zebrafish (Toxicology reports · 2022Article
- Metformin attenuates angiotensin II-induced cardiomyocyte hypertrophy by upregulating the MuRF1 and MAFbx pathway.Experimental and therapeutic medicine · 2021Article
- Haemodynamic dependence of mechano-genetic evolution of the cardiovascular system in Japanese medaka.Journal of the Royal Society, Interface · 2021Article
- Phenanthrene alters the electrical activity of atrial and ventricular myocytes of a polar fish, the Navaga cod.Aquatic toxicology (Amsterdam, Netherlands) · 2021Article
- Heart Failure and PAHs, OHPAHs, and Trace Elements Levels in Human Serum: Results from a Preliminary Pilot Study in Greek Population and the Possible Impact of Air Pollution.Molecules (Basel, Switzerland) · 2021Article
- Phenanthrene impacts zebrafish cardiomyocyte excitability by inhibiting IKr and shortening action potential duration.The Journal of general physiology · 2021Article
- The Zinc Nutritional Immunity ofFrontiers in immunology · 2021Article
- MicroRNA (miRNA) Differential Expression and Exposure to Crude-Oil- Related Compounds.MicroRNA (Shariqah, United Arab Emirates) · 2021Review
- The effects of phenanthrene exposure on Treg and Th17 cells related cytokines in female rats.Toxicology research · 2020Article
- Polyaromatic hydrocarbons in pollution: a heart-breaking matter.The Journal of physiology · 2020Review
- Article
- Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles.Environmental health : a global access science source · 2019Review
- The MicroRNA Family Both in Normal Development and in Different Diseases: The miR-17-92 Cluster.BioMed research international · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence indicates that there is an emerging link between environmental pollution and cardiac hypertrophy, while the mechanism is unclear. The objective of this study was to examine whether phenanthrene (Phe) could cause cardiac hypertrophy, and elucidate the molecular mechanisms involved. We found that: 1) Phe exposure increased the heart weight and cardiomyocyte size of rats; 2) Phe exposure led to enlarged cell size, and increased protein synthesis in H9C2 cells; 3) Phe exposure induced important markers of cardiac hypertrophy, such as atrial natriuretic peptide, B-type natriuretic peptide, and c-Myc in H9C2 cells and rat hearts; 4) Phe exposure perturbed miR-133a, CdC42 and RhoA, which were key regulators of cardiac hypertrophy, in H9C2 cells and rat hearts; 5) Phe exposure induced DNA methyltransferases (DNMTs) in H9C2 cells and rat hearts; 6) Phe exposure led to methylation of CpG sites within the miR-133a locus and reduced miR-133a expression in H9C2 cells; 7) DNMT inhibition and miR-133a overexpression could both alleviate the enlargement of cell size and perturbation of CdC42 and RhoA caused by Phe exposure. These results indicated that Phe could induce cardiomyocyte hypertrophy in the rat and H9C2 cells. The mechanism might involve reducing miR-133a expression by DNA methylation.
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Registered trials
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