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Fig. 8 | Particle and Fibre Toxicology

Fig. 8

From: Long-term PM2.5 exposure disrupts corneal epithelial homeostasis by impairing limbal stem/progenitor cells in humans and rat models

Fig. 8

Mechanism overview: Long-term PM2.5 exposure impairs limbal stem/progenitor cells by disrupting the circadian rhythm and their stem cell niche. Long-term PM2.5 exposure destructs the limbal microenvironment manifested as decreased vascular density and permeability, decreased corneal subbasal nerve fiber, and enhanced inflammation, which perturbs the circadian rhythm of LSPCs and causes LSPCs dysregulation. Corneal epithelial homeostasis can no longer be maintained, and a variety of corneal diseases ultimately occur. In addition, short-term microenvironmental responses might be involved in the activation of LSPCs by circadian perturbations to promote the maintenance of corneal epithelial homeostasis. LSPCs: Limbal stem/progenitor cells

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