ArticleFrontiers in medicine2025
Polystyrene microplastics impair the function of human retinal microvascular endothelial cells and pericytes and increase vascular permeability
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- Effects of micro and nano plastics on renal health.World journal of nephrology · 2026Review
- Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways.Particle and fibre toxicology · 2026Review
- From the Gut to the Brain: Microplastic-Associated Neurovascular Dysfunction and Implications for Stroke Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- An overview of research on the association between microplastics and central nervous system disorders.Frontiers in public health · 2025Review
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Polystyrene (PS) microplastics are among the most prevalent types of microplastics responsible for global pollution. Although numerous studies have investigated the effects of PS on various organs, such as the heart, lungs, liver, kidneys, nervous system, and intestines, its impact on the eyes, particularly the retina, remains largely unexplored. Methods: To assess the effects of PS on retinal pathology, cultured retinal microvascular endothelial cells, pericytes, astrocytes, and microglial cells were exposed to 2 μm PS particles. Cell viability (MTT assay), apoptosis (Annexin V/PI flow cytometry), protein expression (Western blotting), and angiogenesis-related behaviors (tube formation, migration, and permeability assays) were evaluated. Results: PS induced endothelial cell apoptosis by reducing the activity of AKT and ERK1/2, and induced pericyte apoptosis by reducing the activity of AKT. PS also impaired tube formation, migration, and proliferation by reducing AKT and ERK1/2 activity in retinal endothelial cells. In addition, PS induced pericyte apoptosis and increased endothelial permeability. Conclusion: PS may worsen retinopathy by inducing endothelial cell and pericyte apoptosis and by increasing vascular leakage, although it does not promote angiogenesis.
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Registered trials
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