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Purpose. To investigate the influences of atropine on changes in anterior segment geometry, as measured by ultrasound biomicroscopy in children. Methods. A prospective observational study was performed. Anterior segment parameters were obtained by UBM before and after the instillation of 1% atropine. Univariate linear regression was performed to identify the variables contributing to the changes in the trabecular meshwork-iris angle (TIA). Results. The study included 21 boys and 37 girls with a mean age of 10.79 ± 2.53 years. Anterior chamber parameters including the central anterior chamber depth, TIA, angle opening distance at 500 μm from the scleral spur, iris thickness 750 μm and 1500 μm from the scleral spur, trabecular-ciliary angle (TCA), trabecular-ciliary process distance, sclera-iris angle (SIA), and sclera-ciliary process angle significantly increased after cycloplegia ( P < 0.05 ). In contrast, the lens vault, iris cross-sectional area, and maximum ciliary muscle thickness significantly decreased after cycloplegia. Univariate analysis identified the change in TCA and the change in SIA and the TIA before mydriasis as determinants of the change in TIA. Conclusions. Atropine causes statistically significant changes in various anterior segment parameters in children. The change in anterior chamber angle is associated with the change in TCA and the change in SIA and the TIA before mydriasis.

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Choroidal neovascularization (CNV), is a major cause of irreversible blindness among the elderly population in developed countries, which is resulted from subretinal fibrosis without effective therapeutic strategies. Endothelial‐to‐mesenchymal transition (EndMT) of choroidal vascular endothelial cells (CVECs) contributes to subretinal fibrosis. Lycopene (LYC), a non‐pro‐vitamin A carotenoid, plays an anti‐fibrotic role. Herein, we explored the effect and mechanism of LYC on the EndMT of CVECs during CNV. Firstly, LYC inhibited EndMT in hypoxic human choroidal endothelial cells (HCVECs). Meanwhile, LYC inhibited proliferation, androgen receptor (AR) expression and nuclear localization in hypoxic HCVECs. Then LYC‐inhibited AR promotes the activation of microphthalmia‐associated transcription factor (MITF) in hypoxic HCVECs. In addition, LYC down‐regulated AR and induced MITF up‐regulated pigment epithelium‐derived factor (PEDF) transcription and expression in hypoxic HCVECs. Moreover, LYC‐induced PEDF bound to laminin receptor (LR), inhibiting EndMT of hypoxic HCVECs via down‐regulating protein kinase B (AKT)/β‐catenin pathway. In vivo, LYC alleviated mouse laser‐induced subretinal fibrosis secondary to CNV via up‐regulating PEDF without any ocular or systemic toxicity. These results indicate that LYC inhibits EndMT of CVECs via modulating AR/MITF/PEDF/LR/AKT/β‐catenin pathway, showing LYC is a promising therapeutic agent for CNV.