ArticleInternational ophthalmology2025
Upregulated miR-1298-5p sparks inflammatory onset and orchestrates pediatric dry eye disease progression.
Article in International ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeDry eye disease (DED) is a multifactorial chronic ocular surface disorder with increasing annual prevalence in the pediatric population. MicroRNAs serve as biomarkers, yet the mechanistic role of miR-1298-5p in pediatric DED remains unclear. This study aims to investigate the role of miR-1298-5p in PDED and provide new insights into its clinical treatment.
methodsThe study enrolled 71 PDED and 68 healthy controls. Tear miR-1298-5p levels were quantified via RT-qPCR, while ELISA and HPLC measured inflammatory cytokines and serum vitamin A. Pearson correlation analysis evaluated associations between miR-1298-5p expression and inflammatory cytokines and vitamin A levels. Multivariate logistic regression identified independent risk factors for PDED. An in vitro LPS-stimulated PDED model was established in human corneal epithelial cells, followed by miR-1298-5p inhibition to assess apoptosis and inflammation.
resultsInflammatory factors, vitamin A levels, and outdoor activity time were significant risk factors for pediatric PDED. The level of miR-1298-5p in the tears of children with PDED is 1.5 times higher than that in the healthy control group (P < 0.001). It shows a strong positive correlation with IL-6 (r = 0.687), TNF-α (r = 0.604), and IL-1β (r = 0.610), and a negative correlation with vitamin A (r = -0.566). Multivariate analysis showed that miR-1298-5p was the strongest predictor of PDED (OR = 17.08, 95% CI 6.13-47.55). In vitro, miR-1298-5p inhibition reduced LPS-induced HCEC apoptosis and inhibited the secretion of IL-6, TNF-α, and IL-1β inflammatory factors.
conclusionmiR-1298-5p emerges as a novel PDED biomarker, correlating with inflammation and vitamin A. It exacerbates corneal damage through apoptotic/inflammatory pathways, offering therapeutic targets and mechanistic insights.
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