ArticleParticle and fibre toxicology2023
Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage.
Article in Particle and fibre toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.
- Mechanism of microplastics in respiratory disease from 2020 to 2024: visualization and bibliometric analysis.Frontiers in medicine · 2025Pooled it
- Article
- Microplastic-Induced DRP1-BAX Interaction Contributes to Mitochondrial Apoptosis in Lung Epithelial Cells.Environment & health (Washington, D.C.) · 2026Article
- Environmentally relevant aged nanoplastics amplify oxidative stress-associated inhalation toxicity and delay lung clearance.Redox biology · 2026Article
- Astragaloside IV mitigates mitochondrial damage and neurological symptoms in rats with cervical spondylotic myelopathy by inhibiting IL-17/TRAF6/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Emerging role of microplastics and nanoplastics in children's health.Pediatric research · 2026Review
- Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways-A Critical Review.Antioxidants (Basel, Switzerland) · 2026Review
- Apical-out airway organoids as a pathophysiological model to study macrophage-mediated epithelial responses to microplastics.Materials today. Bio · 2026Article
- Investigating the microwave degradation of polypropylene microplastics and their impact on human intestinal cell models.Toxicology reports · 2026Article
- Micro-Nanoplastic Exposure and Lung Cancer Biomarkers: The Role of Extracellular Vesicle-Mediated Intercellular Communication.International journal of molecular sciences · 2026Review
- Review
- Ferroptosis and Wnt/β-Catenin Signaling Triggered by Environmentally Relevant Nanoscale Polypropylene Plastics in Human Intestinal Models.ACS environmental Au · 2026Article
- Protein phosphatase 2A/Hedgehog pathway governs efferocytosis of pulmonary macrophages and participates in nanoplastics-induced mouse lung injury.Cell biology and toxicology · 2026Article
- Respiratory risks of microplastics and nanoplastics: Where? What? How?Innovation (Cambridge (Mass.)) · 2026Review
- Chinese cobra (Naja atra) SVPLACommunications biology · 2026Article
- Polystyrene nanoplastics and benzo(a)pyrene synergistically induce lung fibrosis and inflammation via relaxin signalling in mice.Communications biology · 2026Article
- Sesamin Protects Against Polystyrene Microplastics-Induced Lung Injury via Attenuating Bcl2-Mediated Apoptosis.Antioxidants (Basel, Switzerland) · 2026Article
- Micro- and Nanoplastics and Pulmonary Health: The Current State of Research.Microplastics (Basel, Switzerland) · 2026Article
- Polystyrene Nanoparticles Disrupt Oxidative Phosphorylation and Impair Placental Development in Mice.Toxics · 2026Article
- Polystyrene nanoplastics-induced lung epithelial cells ferroptosis promotes pulmonary fibrosis via YY1/FTL axis.Materials today. Bio · 2026Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPolypropylene (PP) is used in various products such as disposable containers, spoons, and automobile parts. The disposable masks used for COVID-19 prevention mainly comprise PP, and the disposal of such masks is concerning because of the potential environmental pollution. Recent reports have suggested that weathered PP microparticles can be inhaled, however, the inhalation toxicology of PP microparticles is poorly understood.
resultsInflammatory cell numbers, reactive oxygen species (ROS) production, and the levels of inflammatory cytokines and chemokines in PP-instilled mice (2.5 or 5 mg/kg) increased significantly compared to with those in the control. Histopathological analysis of the lung tissue of PP-stimulated mice revealed lung injuries, including the infiltration of inflammatory cells into the perivascular/parenchymal space, alveolar epithelial hyperplasia, and foamy macrophage aggregates. The in vitro study indicated that PP stimulation causes mitochondrial dysfunction including mitochondrial depolarization and decreased adenosine triphosphate (ATP) levels. PP stimulation led to cytotoxicity, ROS production, increase of inflammatory cytokines, and cell deaths in A549 cells. The results showed that PP stimulation increased the p-p38 and p-NF-κB protein levels both in vivo and in vitro, while p-ERK and p-JNK remained unchanged. Interestingly, the cytotoxicity that was induced by PP exposure was regulated by p38 and ROS inhibition in A549 cells.
conclusionsThese results suggest that PP stimulation may contribute to inflammation pathogenesis via the p38 phosphorylation-mediated NF-κB pathway as a result of mitochondrial damage.
Indexed as
Identifiers
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.