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Objectives This study aimed to quantitatively evaluate optic nerve head and retinal vascular parameters in children with hyperopia in relation to age and spherical equivalent refraction (SER) using artificial intelligence (AI)-based analysis of colour fundus photographs (CFP).Methods and analysis This cross-sectional study included 324 children with hyperopia aged 3–12 years. Participants were divided into low hyperopia (SER+0.5 D to+2.0 D) and moderate-to-high hyperopia (SER≥+2.0 D) groups. Fundus parameters, such as optic disc area and mean vessel diameter, were automatically and quantitatively detected using AI. Significant variables (p

Background: Vision loss is a leading cause of healthy life loss in late adulthood. We aimed to comprehensively examine the impact of population aging on vision loss prevalence worldwide. Methods: This population-based study used repeated cross-sectional data on vision loss and its related causes from the Global Burden of Disease 2019 study. We investigated the impact of population aging by decomposing changes in vision loss prevalence into contributions of population growth, population aging, and epidemiological rate changes using the latest decomposition method and comparing the net effect of population aging and epidemiological rate changes. Results: The global vision loss prevalence attributed to population aging increased from 1991 to 2019, reaching 183.37 million in 2019. In relation to the 19 vision loss causes, the greatest increase in population aging-attributed vision loss prevalence was observed for near vision loss, refraction disorders, and cataract, whereas the contributions of glaucoma, diabetic retinopathy, and age-related macular degeneration were not substantial. The impact of population aging on vision loss prevalence varied greatly worldwide based on development levels. However, in most countries, the increase in vision loss prevalence caused by population aging exceeded far and could not be offset by epidemiological rate variations. Conclusions: With the aging of the population, vision loss has become one of the most serious public health concerns. It is imperative that policy makers invest more in vision health preventive medicine and implement proven, cost-effective interventions to combat the epidemic of vision loss as the population ages.

Abstract Background Neuroinflammation and mitochondrial dysfunction play crucial roles in retinal ischemia and reperfusion (IR) injury. Recent studies have identified mitochondrial function as a promising target for immunomodulation. Empagliflozin (EMPA), an anti-diabetic drug, has exhibited great potential as both an anti-inflammatory agent and a protector of mitochondrial health. This study aimed to assess the therapeutic efficacy of EMPA in retinal IR injury. Methods To evaluate the protective effects of EMPA, the drug was injected into the vitreous body of mice post-retinal IR. Single-cell RNA sequencing (scRNA-seq) analysis was conducted to uncover the underlying mechanisms, and the results were further validated through in vivo and in vitro experiments. Results EMPA effectively protected retinal ganglion cells (RGCs) from IR injury by attenuating local retinal inflammation. The scRNA-seq analysis revealed that EMPA downregulated the nucleotide-binding domain and leucine-rich repeat containing protein 3 (NLRP3) signaling pathway and restored mitochondrial dynamics by upregulating the expression of mitochondrial fusion-related genes, Mitofusin 1 (Mfn1) and optic atrophy 1 (Opa1). These findings were further corroborated by Western blotting. In vitro experiments provided additional insights, demonstrating that EMPA suppressed lipopolysaccharide (LPS)-induced cell inflammation and NLRP3 inflammasome activation. Moreover, EMPA enhanced mitochondrial fusion, neutralized mitochondrial reactive oxygen species (mtROS), and restored mitochondrial membrane potential (MMP) in BV2 microglia. Notably, genetic ablation of Mfn1 or Opa1 abolished the anti-inflammatory effects of EMPA. Conclusions Our findings highlight the positive contribution of Mfn1 and Opa1 to the anti-inflammatory therapeutic effect of EMPA. By restoring mitochondrial dynamics, EMPA effectively mitigates microglia-mediated neuroinflammation and prevents RGC loss in retinal IR injury.