Hong Li

Glaucoma consists of a group of neurodegenerative diseases characterized by retinal ganglion cell degeneration, in which Müller cells are increasingly recognised as drivers of neuroinflammation. A ketogenic diet (KD) elevates circulating β‑hydroxybutyrate (BHB) and exhibits benefits in other neurodegenerative disorders; however, its role in glaucoma remains poorly understood. In the present study, an experimental autoimmune glaucoma (EAG) mouse model was established and primary Müller cells were cultured. Using spectrophotometry, optical coherence tomography and immunofluorescence, serum ketone body levels were found to be significantly lower in both patients with primary open‑angle glaucoma and EAG mice, independent of intraocular pressure. In vitro and in vivo experiments showed that KD increased BHB levels and ketone body metabolism, suppressed Müller cell activation and reduced retinal neuroinflammation. In addition, 4D data‑independent acquisition proteomic analysis and subsequent validation revealed that FOXO3A acetylation and FOXO3A and metallothionein 2A upregulation were regulated in the retina and Müller cells. These findings suggest that impaired ketone body metabolism occurs in glaucoma and that KD‑mediated neuroprotection is associated with altered FOXO3A acetylation. The present study highlighted an association between ketone metabolism and immune regulation in glaucoma, providing evidence for Müller cell phenotypic modulation and supported further investigation of KD as a potential neuroprotective adjunct therapy for glaucoma.

Glaucoma is a leading cause of irreversible blindness characterized by the progressive degeneration of retinal ganglion cells (RGCs), largely driven by persistent oxidative stress. While selenium (Se) offers robust endogenous antioxidant defense, the severe toxicity and narrow therapeutic window of inorganic selenium strictly limit its application. To overcome this critical bottleneck, chitosan-functionalized selenium nanoparticles (CS-SeNPs) are engineered. This strategic nanomodification effectively shields the inherent toxicity of free selenium while conferring exceptional colloidal stability and superior biocompatibility. Clinically, systemic Se levels in patients with primary open-angle glaucoma (POAG) are found to be significantly diminished compared to healthy controls. Mechanistically, transcriptome sequencing reveals that CS-SeNPs function through the PI3K/Akt pathway to upregulate the downstream Nrf2/HO-1 antioxidant axis, effectively reducing intracellular oxidative stress and apoptosis. In vivo, an intravitreal administration strategy for CS-SeNPs is established. In a rat model of acute ocular hypertension (AOH), this targeted local delivery markedly reduces oxidative damage, preserves retinal hierarchical architecture, and profoundly restores visual electrophysiological function. These findings identify systemic Se deficiency as a clinical hallmark of POAG and demonstrate that intravitreal CS-SeNPs offer a highly promising, intraocular pressure-independent nanotherapeutic strategy for glaucomatous neuroprotection.

This study aims to investigate how selective intrinsically photosensitive retinal ganglion cells (ipRGCs) ablation regulates axial length (AL) and scleral remodeling to modulate myopia progression. Three-week-old tri-colored guinea pigs were randomly assigned to five experimental groups, with form-deprivation myopia (FDM) models receiving intravitreal melanopsin-saporin (MEL-SAP) injections. Longitudinal ocular biometrics were recorded. Molecular analyses (Western blot, RT-qPCR) quantified expression of retina-, choroid-, and sclera-related factors. Structural changes were assessed via immunohistochemistry, optical coherence tomography (OCT; choroidal/scleral thickness), and Masson’s trichrome staining (scleral collagen organization). In FDM models, melanopsin expression was elevated. MEL-SAP injection shortened AL but exacerbated early refractive error, likely through corneal alterations. This treatment attenuated AL elongation and delayed refractive progression in FDM+MEL-SAP groups versus FDM alone. Molecular analyses indicated suppression of FDM-induced scleral remodeling markers and choroidal hypoxia indicators following selective ipRGCs ablation. The extracellular regulated kinase (ERK) activation rescued these effects, establishing microtubule-associated protein kinase (MAPK) signaling's mechanistic role. Choroidal perfusion experiments confirmed selective ipRGC ablation's primary action through the retinal-choroidal-scleral(RCS) axis. Consequently, selective ipRGCs ablation inhibits the AL in myopia through the choroid/MAPK signaling axis, refining the retinal mechanism of myopia development.

Background: Glaucoma is a leading cause of irreversible blindness, with a rising global prevalence, driving an increased public search for health information online. Online video platforms, such as Douyin and Bilibili, have become key channels for health communication. However, the quality and reliability of glaucoma-related content on these platforms remain unclear, raising concerns regarding potential misinformation. Methods: On 22 October 2025, the top 100 Chinese-language videos of glaucoma from Douyin and Bilibili were systematically collected. The video metadata and engagement metrics were recorded. Quality and reliability were assessed using the Global Quality Score (GQS), modified Decision-making Information Support Criteria for Evaluating the Reliability of Nonrandomized Studies (mDISCERN), JAMA (Journal of the American Medical Association) benchmark criteria, and Patient Education Materials Assessment Tool (PEMAT) for Audio Visual Content. Statistical analysis including Spearman correlation was used to examine the relationships between video variables and quality scores. Results: Douyin videos exhibited significantly higher user interaction (likes, comments, shares, and saves) than Bilibili videos. However, the Bilibili videos demonstrated significantly higher median scores for GQS and PEMAT actionability. Videos from professional sources, particularly institutions, and those focusing on disease prevention or using expert monologue/visual aids consistently showed superior quality and reliability across all the assessment tools. Spearman correlation revealed that longer video duration was positively correlated with higher GQS, mDISCERN, and PEMAT understandability scores, whereas fewer comments were negatively correlated with these scores. Conclusions: The overall quality and reliability of glaucoma-related online videos from Douyin and Bilibili were suboptimal. Content from nonprofessional sources was problematic. These findings highlight the need for public vigilance when consuming health information on such platforms, and underscore the importance of encouraging greater involvement from healthcare professionals in creating accurate, high-quality educational content.

Purpose: To compare the efficacy of topical levofloxacin and gatifloxacin at different durations in reducing conjunctival bacteria. Methods: In total, 285 patients (290 eyes) scheduled to undergo ophthalmic surgery were divided into 6 groups to receive either gatifloxacin or levofloxacin eye drops for 1 day (12 times/day), 2 days (6 times/day), or 3 days (4 times/day) before surgery. Conjunctival sac specimens were collected from all patients before treatment (T0) and after treatment (T1). All specimens were inoculated onto Columbia blood agar plates. Results: Before treatment, the culture positivity rate was 50.34% for 290 samples, and after treatment, the culture positivity rate was 11.72% (P < 0.05). Corynebacterium spp. and Staphylococcus spp. were the most predominantly detected microbial groups before and after treatment. The bacterial eradication rate was higher in the gatifloxacin group (87.01%) than in the levofloxacin group (81.15%). There was no difference in culture positivity between gatifloxacin 1-, 2-, and 3-day groups (P > 0.05). The culture positivity rate was significantly higher in the levofloxacin 1-day group than in the 2- and 3-day groups (P < 0.05). Both drugs were effective in removing gram-positive bacillus at different durations (P < 0.01), but only the levofloxacin treatment for 3 days significantly reduced the positive cultures of gram-positive cocci in the conjunctival sac (P < 0.05). Conclusions: Our study demonstrated that preoperative use of levofloxacin to prevent infection takes at least 2-3 days, and 1 day is a sufficient duration for topical gatifloxacin to significantly reduce conjunctival bacterial flora.

Glaucoma is a leading cause of irreversible blindness, characterized by progressive retinal ganglion cells (RGCs) loss. Increasing evidence links microglial activation and lipid metabolism dysregulation to neurodegeneration. However, the role of microglial lipid metabolic reprogramming in disease pathogenesis remains unclear. This study finds that microglia in an acute ocular hypertension (AOH) model exhibit abnormal lipid droplet accumulation, downregulation of low‐density lipoprotein receptor‐related protein 1 (LRP1), and a shift toward a pro‐inflammatory M1 phenotype. Importantly, serum samples from glaucoma patients reveal significantly reduced LRP1 levels compared to controls. To restore lipid homeostasis, this study develops alpinetin‐loaded PLGA nanoparticles (AlpNPs), which demonstrate efficient microglial uptake and sustained release. AlpNPs reduced intracellular lipid accumulation, promoted M2 polarization, and suppressed microglial proliferation and migration. Mechanistically, AlpNPs directly bind to LRP1 and enhance its interaction with PPARγ, thereby activating the downstream LXRα‐ABCA1 pathway, which is pivotal for cholesterol efflux and anti‐inflammatory responses. Knockdown of LRP1 abolished the protective effects of AlpNPs, confirming its essential role in mediating metabolic reprogramming. In vivo, intravitreal injection of AlpNPs significantly attenuates retinal inflammation and preserves RGCs in AOH. These findings identify microglial lipid metabolic dysfunction as a key driver in glaucoma and highlight LRP1‐targeted nanotherapy as a promising strategy for neuroprotection.