ArticleParticle and fibre toxicology2023
Long-term PM2.5 exposure disrupts corneal epithelial homeostasis by impairing limbal stem/progenitor cells in humans and rat models.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Association between air pollutant exposure and ocular surface, anterior and middle segment and fundus eye diseases: epidemiological and mechanism evidence.Eye (London, England) · 2026Review
- Corneal biomechanical cues mediated by PAI-2: the origin of PM2.5-induced corneal disease.EMBO molecular medicine · 2026Article
- Long-term exposure to fine particulate matter and its constituents is related to self-reported visual impairment among middle-aged and older adults: a longitudinal study in China.BMC public health · 2025Article
- Circadian disruption and ROS-NLRP3 signaling mediate sleep deprivation-enhanced silica nanoparticle toxicity in lacrimal glands.Journal of nanobiotechnology · 2025Article
- Wildfire Smoke Induces Eye Surface Inflammation and Tear Film Changes in a Human Experimental Model.Translational vision science & technology · 2025Article
- SLC6A6-Mediated Taurine Uptake Sustains Corneal Epithelial Stem/Progenitor Cell Function to Counteract Age-Related Dysfunction.Investigative ophthalmology & visual science · 2025Article
- Relationship between long-term PM2.5 exposure and myopia prevalence in adults: analysis of the Korea National Health and Nutrition Examination Survey-Air Pollution Linked Data, 2020.Annals of occupational and environmental medicine · 2025Article
- Rebamipide Enhances Pathogen Defense and Mitigates Inflammation in a Particulate Matter-Induced Ocular Surface Inflammation Rat Model.International journal of molecular sciences · 2025Article
- The nonlinear impact of air pollutants and solar radiation exposure on the risk of hospitalisation for pterygium among adults in Shanghai, China: a time series analysis.Journal of global health · 2025Article
- Ozone exposure and increased risk of age-related macular degeneration: Evidence from nationwide cohort and toxicological studies.Innovation (Cambridge (Mass.)) · 2025Article
- Microplastics and nanoplastics in the ocular environment: Pathways, toxic effects, and future challenges.Current research in toxicology · 2025Review
- Therapeutic Potential of Herbal Medicines in Combating Particulate Matter (PM)-Induced Health Effects: Insights from Recent Studies.Antioxidants (Basel, Switzerland) · 2024Review
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundLimbal stem/progenitor cells (LSPCs) play a crucial role in maintaining corneal health by regulating epithelial homeostasis. Although PM2.5 is associated with the occurrence of several corneal diseases, its effects on LSPCs are not clearly understood.
methodsIn this study, we explored the correlation between PM2.5 exposure and human limbal epithelial thickness measured by Fourier-domain Optical Coherence Tomography in the ophthalmologic clinic. Long- and short-term PM2.5 exposed-rat models were established to investigate the changes in LSPCs and the associated mechanisms.
resultsWe found that people living in regions with higher PM2.5 concentrations had thinner limbal epithelium, indicating the loss of LSPCs. In rat models, long-term PM2.5 exposure impairs LSPCs renewal and differentiation, manifesting as corneal epithelial defects and thinner epithelium in the cornea and limbus. However, LSPCs were activated in short-term PM2.5-exposed rat models. RNA sequencing implied that the circadian rhythm in LSPCs was perturbed during PM2.5 exposure. The mRNA level of circadian genes including Per1, Per2, Per3, and Rev-erbα was upregulated in both short- and long-term models, suggesting circadian rhythm was involved in the activation and dysregulation of LSPCs at different stages. PM2.5 also disturbed the limbal microenvironment as evidenced by changes in corneal subbasal nerve fiber density, vascular density and permeability, and immune cell infiltration, which further resulted in the circadian mismatches and dysfunction of LSPCs.
conclusionThis study systematically demonstrates that PM2.5 impairs LSPCs and their microenvironment. Moreover, we show that circadian misalignment of LSPCs may be a new mechanism by which PM2.5 induces corneal diseases. Therapeutic options that target circadian rhythm may be viable options for improving LSPC functions and alleviating various PM2.5-associated corneal diseases.
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