ArticleCardiovascular toxicology2024
Potential Effects of Orally Ingesting Polyethylene Terephthalate Microplastics on the Mouse Heart.
Article in Cardiovascular toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- From pollution to palpitations: the heart's silent battle with microplastics.BMC cardiovascular disorders · 2025Pooled it
- Micro- and Nanoplastics in Cardiovascular Toxicology: Human Tissue Detection, Clinical Phenotypes, and Adverse Outcome Signals.Cardiovascular toxicology · 2026Review
- Micro- and Nanoplastics as Potential Drivers of Dilated Cardiomyopathy.Life (Basel, Switzerland) · 2026Review
- Microplastics and Nanoplastics in Cardiovascular Disease: An Emerging Cardiovascular Risk Factor.Cardiovascular toxicology · 2026Review
- Small particles, large questions: unravelling the toxicity and potential health risks of PET micro-/nanoplastics.Particle and fibre toxicology · 2026Review
- Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways.Particle and fibre toxicology · 2026Review
- Evaluation of Polystyrene Nanoplastics Induced Cardiotoxicity Under Different Dietary Patterns in Mice.Toxics · 2025Article
- Review
- Antioxidant Intervention Against Microplastic Hazards.Antioxidants (Basel, Switzerland) · 2025Review
- A Workflow for Assessing Particle Counts of Mixed Micro- and Nanoplastics in Exposed Laboratory Animals.Nanomaterials (Basel, Switzerland) · 2025Article
- Organ-specific accumulation and toxicity analysis of orally administered polyethylene terephthalate microplastics.Scientific reports · 2025Article
- Developing a feasible fast-track testing method for developmental neurotoxicity studies: alternative model for risk assessment of micro- and nanoplastics.Frontiers in toxicology · 2025Review
- Influence of micro- and nanoplastics on mitochondrial function in the cardiovascular system: a review of the current literature.Physiological research · 2024Review
- Micro(nano)plastics: an Emerging Burden for Human Health.International journal of biological sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyethylene terephthalate microplastics (PET MPs) are widespread in natural environment, and can enter organisms and accumulate in the body, but its toxicity has not been well studied. Therefore, in order to investigate the toxic effects of PET microplastics on mammals, this study investigated the toxic effects of PET MPs on ICR mice and H9C2 cells by different treatment groups. The results indicated the cardiac tissue of mice in the PET-H (50 µg/mL) group showed significant capillary congestion, myocardial fiber breakage, and even significant fibrosis compared to the PET-C (control) group (P < 0.01). Results of the TUNEL assay demonstrated significant apoptosis in myocardial tissue in the PET-H and PET-M (5 µg/mL) groups (P < 0.01). Meanwhile, Western blotting showed increased expression of the apoptosis-related protein Bax and decreased expression of PARP, caspase-3, and Bcl-2 proteins in both myocardial tissues and H9C2 cells. In addition, flow cytometry confirmed that PET MPs decreased the mitochondrial membrane potential and apoptosis in H9C2 cells; however, this trend was reversed by N-acetylcysteamine application. Moreover, PET MP treatment induced the accumulation of reactive oxygen species (ROS) in H9C2 cells, while the MDA level in the myocardial tissue was elevated, and the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were decreased (P < 0.01), indicating a change in the redox environment. In conclusion, PET MPs promoted cardiomyocyte apoptosis by inducing oxidative stress and activating mitochondria-mediated apoptotic processes, ultimately leading to myocardial fibrosis. This study provides ideas for the prevention of PET MP toxicity and promotes thinking about enhancing plastic pollution control.
Indexed as
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What OpenQuestion holds
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.