ArticleMedical science monitor : international medical journal of experimental and clinical research2017
Cardiotoxicity and Mechanism of Particulate Matter 2.5 (PM2.5) Exposure in Offspring Rats During Pregnancy.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Effect of Fine Particulate Matter Exposure on Liver Enzymes: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2023Pooled it
- Maternal exposure to urban particulate matter induces cardiac developmental toxicity in zebrafish offspring by disrupting mitochondrial homeostasis.Journal of advanced research · 2026Article
- Gestational exposure to micro and nanoplastics differentially impacts cardiac development and function in male and female rats throughout the lifespan.Toxicology and applied pharmacology · 2025Article
- MiR221/222 in the conditioned medium of adipose-derived stem cells attenuates particulate matter and high-fat diet-induced cardiac apoptosis.Stem cell research & therapy · 2025Article
- Fine particulate matter‑induced cardiac developmental toxicity (Review).Experimental and therapeutic medicine · 2025Review
- [Metformin ameliorates PM2.5-induced functional impairment of placental trophoblasts by inhibiting ferroptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- An Overview of Adverse Outcome Pathway Links between PMEnvironment & health (Washington, D.C.) · 2024Review
- Article
- Maternal exposure to PM2.5 induces the testicular cell apoptosis in offspring triggered by the UPR-mediated JNK pathway.Toxicology research · 2022Article
- Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology.American journal of physiology. Heart and circulatory physiology · 2020Review
- Real-Ambient Particulate Matter Exposure-Induced Cardiotoxicity in C57/B6 Mice.Frontiers in pharmacology · 2020Article
- Vitamin D deficiency enhances insulin resistance by promoting inflammation in type 2 diabetes.International journal of clinical and experimental pathology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to investigate the cardiotoxicity and mechanism of particulate matter 2.5 (PM2.5) exposure on offspring rats during pregnancy. MATERIAL AND METHODS Wistar rats were used to establish a PM2.5 exposure animal model during pregnancy, and they were divided into a control group, a low-dose group, a middle-dose group, and a high-dose group according to PM2.5 exposure dose. The pathological changes of heart tissue, the rate of myocardial cell apoptosis, the levels of LDH, AST, and CM-KB in serum, and the difference in mitochondrial fusion genes (OPA1 and Mfn1) and mitochondrial genes (Drp1 and Fis1) were compared among groups. RESULTS The arrangement of myocardial fibers in offspring mice of PM2.5 exposure groups became disordered, the shape of some cardiomyocytes became irregular, and some staining darker nuclei appeared. The apoptotic rates of myocardium in offspring rats exposed to PM2.5 were (12.61±0.93)% in the low-dose group, (25.14±1.53)% in the middle-dose group, and (30.13±1.50)% in the high-dose group, which were all significantly higher than in the control group (9.12±0.80)% (P<0.05). The levels of LDH, AST, and CM-KB and the expression of OPA1, Mfn1, Drp1, and Fis1 in offspring mice of PM2.5 exposure groups increased with the increase of PM2.5 exposure dose, and were significantly higher than that of the control group (P<0.05). CONCLUSIONS The mitochondria of the offspring mice were damaged due to the abnormal expression of mitochondrial fusion/splicing gene by PM2.5 exposure during pregnancy, and the hearts of offspring mice were damaged due to damaged mitochondria.
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