Experimental eye research最新文献

{"title":"The pathogenicity of a novel frame-shift variant c.2321delC of PROM1 in an autosomal recessive cone-rod dystrophy pedigree may be associated with augment of autophagy","authors":"Chenyu Wu ,&nbsp;Lujia Zhang ,&nbsp;Qingge Guo ,&nbsp;Ya Li ,&nbsp;Ruiqi Qiu ,&nbsp;Shun Yao ,&nbsp;Bo Lei","doi":"10.1016/j.exer.2025.110453","DOIUrl":"10.1016/j.exer.2025.110453","url":null,"abstract":"<div><div><em>PROM1</em> gene mutations are increasingly recognized as significant contributors to inherited retinal diseases, demonstrating considerable heterogeneity in mutation loci and types. In our investigation of a Chinese pedigree presenting with autosomal recessive cone-rod dystrophy, we identified two compound heterozygous frame-shift variants of the <em>PROM1</em> gene: c.1645-1648del (p.K549Qfs∗3) and c.2321delC (p.A774Vfs∗2). We focused on elucidating the pathogenicity and underlying mechanisms of the novel c.2321delC variant. Following the American College of Medical Genetics and Genomics (ACMG) standards and guidelines, this novel variant was assessed as likely pathogenic. Cellular assays demonstrated that the mutated protein exhibited aberrant subcellular localization and decreased stability compared to wild-type counterparts. Notably, cellular models revealed significant autophagic activation evidenced by elevated LC3II/I ratios, while apoptosis markers remained unaffected. Despite preserved apoptotic pathways, the variant induced marked cellular viability impairment.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110453"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144134209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in single-cell sequencing of retinal vein occlusion or ischemic hypoxic retinopathy","authors":"Yanbing Feng,&nbsp;Yibo Wu,&nbsp;Yixing Zhu,&nbsp;Yanyan He,&nbsp;Wenqing Weng","doi":"10.1016/j.exer.2025.110436","DOIUrl":"10.1016/j.exer.2025.110436","url":null,"abstract":"<div><div>Retinal vein occlusion (RVO) and ischemic hypoxic retinopathy (IHR) are leading cause of irreversible vision loss worldwide, compelled by complex microvascular dysfunction, neuroinflammation, and tissue hypoxia. Despite advances in imaging and treatment, a comprehensive understanding of cellular and molecular heterogeneity underlying these pathologies remains limited. Recently, single-cell RNA sequencing (scRNA-seq) has emerged as a transformative technology, enabling unprecedented resolution of cellular dynamics, transcriptomic landscapes, and intracellular communication within the retina. Single-cell technologies continue to evolve, they are poised to revolutionize our understanding of retinal vascular diseases, ultimately paving the way for precision diagnostics and targeted interventions. This technique has revolutionized our understanding regarding complex biological systems and enables proper analysis of cellular heterogeneity. This review highlights the recent progress for the application SCS to dissect the pathophysiology of RVO and IHR. Moreover, current study summarizes findings on altered gene expression endothelial cells, Muller glia, micro glia and photoreceptors under ischemic and hypoxic stress, shedding light on potential therapeutic targets and biomarkers. Furthermore, this study explores the integration of snRNA-seq, spatial transcriptomics, and multi-omics approaches to enhance the spatial and temporal mapping of retinal responses. Additionally, discuss the current challenges, including sample preservation, retinal cell-type annotation, and cross-species translation, while offering insights into future directions such as personalized medicine and regenerative strategies. This paper aims to provide clinicians and researchers with a comprehensive update on the rapidly expanding frontier of single-cell analysis in retinal ischemic diseases.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110436"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lycium barbarum glycopeptide alleviates retinal inflammation by suppressing microglial M1 polarization via NF-κB/MAPK pathways","authors":"Yiwen Ou ,&nbsp;Yinhua Huang ,&nbsp;Xu Yang ,&nbsp;Lian Li ,&nbsp;Rangsheng Mei ,&nbsp;Zhexiong Yu ,&nbsp;Kwok-Fai So ,&nbsp;Jiansu Chen ,&nbsp;Jacey Hongjie Ma ,&nbsp;Shibo Tang","doi":"10.1016/j.exer.2025.110452","DOIUrl":"10.1016/j.exer.2025.110452","url":null,"abstract":"<div><div><em>Lycium barbarum</em> glycopeptide (LBGP) is a known glycoconjugate with various pharmacological benefits, notably anti-inflammatory properties, though its impact on retinal inflammatory conditions is not fully understood. This research evaluated the impact of LBGP on retinal inflammation using a diabetic retinopathy (DR) mouse model induced by streptozotocin (STZ), along with LPS/IFN-γ (L/I)-stimulated BV2 microglia and primary retinal microglia. In vivo, administration of LBGP effectively enhances retinal thickness, structure, and function in diabetic mice. Additionally, it prevents microglial activation and inflammation. In vitro, LBGP pretreatment significantly reversed L/I-induced morphological alterations in microglial area, perimeter, Feret's diameter, and roundness. LBGP significantly alleviated L/I-induced microglial activation in primary and BV2 microglia. LBGP shifted M1 pro-inflammatory phenotype to M2 anti-inflammatory phenotype by downregulating M1 markers (IL-6, IL-1β, iNOS, COX2, CD86, and CD16) and upregulating M2 markers (CD206 and arginase 1). Additionally, LBGP reduced the upregulation of NF-κB and MAPK pathways in L/I-stimulated BV2 microglial cells. Our study suggests that LBGP protects against microglial overactivation and diminishes the secretion of inflammatory molecules from microglia in vivo and vitro, potentially through attenuation of the NF-κB and MAPK signaling pathways.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110452"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning Reveals ATM and CNOT6L as critical factors in Cataract pathogenesis","authors":"Peng Qi ,&nbsp;Songhao Zhang ,&nbsp;Wenbing Guo ,&nbsp;Chao Liu","doi":"10.1016/j.exer.2025.110448","DOIUrl":"10.1016/j.exer.2025.110448","url":null,"abstract":"<div><h3>Objective</h3><div>Cataract, a common age-related blinding eye disease, has a complex pathogenesis. This study aims to identify key genes and potential mechanisms associated with cataracts, offering new targets and insights for its prevention and treatment.</div></div><div><h3>Methods</h3><div>Transcriptomic data analysis and machine learning identified ATM serine/threonine kinase (ATM) and CCR4-NOT transcription complex subunit 6 like (CNOT6L) as key differential genes. Their roles in oxidative stress and apoptosis were validated using overexpression experiments in a cataract cell model. Immune-related analyses explored their regulatory effects on the immune microenvironment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed potential mechanisms. In addition, in vitro experiments were conducted to evaluate the effects of ATM and CNOT6L overexpression on cell proliferation, oxidative stress, and apoptosis in lens epithelial cells.</div></div><div><h3>Results</h3><div>We identified 14 aging-associated differentially expressed genes, and ATM and CNOT6L were screened as key genes through machine learning and external dataset validation. KEGG pathway analysis indicated their involvement in base excision repair, ERBB signaling, and fatty acid metabolism pathways. Immune infiltration analysis revealed that ATM and CNOT6L positively correlated with CD8 T cells and B cells, and negatively correlated with regulatory T cells (Tregs), natural killer (NK) cells, and M1 macrophages. In vitro, overexpression of ATM and CNOT6L in cataract cell models promoted cell proliferation, inhibited apoptosis, reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and enhanced glutathione peroxidase (GSH-PX) activity.</div></div><div><h3>Conclusion</h3><div>ATM and CNOT6L play protective roles in cataract progression by reducing oxidative stress, inhibiting apoptosis, and regulating the immune microenvironment. They represent promising molecular targets for cataract prevention and treatment.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110448"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRB1 mutations cause structural and molecular defects in patient-derived retinal pigment epithelium cells","authors":"Yini Wang ,&nbsp;Yuqin Liang ,&nbsp;Yalan Zhou ,&nbsp;Zekai Cui ,&nbsp;Jianing Gu ,&nbsp;Siqi Xiong ,&nbsp;Jiansu Chen","doi":"10.1016/j.exer.2025.110445","DOIUrl":"10.1016/j.exer.2025.110445","url":null,"abstract":"<div><div>Mutations in the <em>CRB1</em> gene can cause retinitis pigmentosa (RP), Leber congenital amaurosis, and other retinopathies, with retinal pigment epithelium (RPE) being a primary affected cell type. However, the effects of <em>CRB1</em> variants on RPE cells remain poorly defined. Here, for the first time, we report an in vitro model of patient-specific RPE cells carrying the <em>CRB1</em> mutations (c.2249G &gt; A and c.2809G &gt; A) to study <em>CRB1</em>-associated RP disease. The patient-derived RPE cells exhibited irregular cell morphology, sparse apical microvilli, abnormal tight junctions, and reduced expression of RPE markers. We also observed that impaired barrier function and phagocytosis lead to increased apical-to-basal movement of fluorescent molecules in disease RPE cells. Notably, transcriptomic analysis revealed decreased expression of cell junction-related genes. In addition, aggregated RPE cells on polydimethylsiloxane (PDMS) microwells significantly enhanced RPE phenotype and cell survival, which was associated with anti-epithelial-mesenchymal transition, anti-aging, and anti-apoptosis. In this study, our results reveal that <em>CRB1</em>-mutated RPE cells generated using RP patient-derived iPSCs could recapitulate the genotype-phenotype features of the disease and provide insights into the pathogenesis of <em>CRB1</em>-associated RPE cells. In addition, our study developed a cell aggregation culture method based on PDMS microwell platforms for the production of highly active and mature iPSC-derived RPE cells.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110445"},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Whole genome sequencing-based prediction of antibiotic-resistance of ocular Staphylococcus aureus across six continents","authors":"Jiawei Shen,&nbsp;Muhammad Yasir,&nbsp;Mark Willcox","doi":"10.1016/j.exer.2025.110425","DOIUrl":"10.1016/j.exer.2025.110425","url":null,"abstract":"<div><div><em>Staphylococcus aureus</em> is a leading cause of ocular infections, resulting in vision loss in severe cases. Understanding the antibiotic resistance profiles of ocular <em>S. aureus</em> can help customize treatments. However, there is a lack of global data on the resistance patterns of ocular isolates and comparative regional analyses. Hence, WGS data from 195 ocular <em>S. aureus</em> isolates across six continents were analysed to identify antibiotic resistance genes (ARGs) and predict antibiotic resistance phenotypes in this study. A total of 40 ARGs were detected, involving resistance mechanisms against aminoglycosides, beta-lactams, macrolide-lacosamide-streptogramin B (MLS_B), glycopeptides, tetracyclines, other antibiotic classes, and efflux pump regulators. Notably, the prevalences of ARGs associated with efflux pump regulators and beta-lactams were particularly high (&gt;80 %). Resistance to 45 antibiotics was predicted across the isolates, with 51 % identified as multidrug-resistant (MDR), while only 8 % were predicted to be fully susceptible to all predicted antibiotics. Regional data varied, with isolates from North America and Asia exhibiting the most extensive resistance patterns, showing predicted resistance to 45 and 41 antibiotics, respectively. In contrast, Oceanian isolates were predicted to be resistant to only 14 antibiotics. Beta-lactams showed the highest predicted resistance prevalence among all antibiotic classes. Notably, North American isolates showed markedly higher resistance to MLS_B antibiotics. A high proportion of cloud genes highlights the need for monitoring regional resistance. This study provides antibiotic resistance profiles among ocular <em>S. aureus</em> using WGS prediction, emphasizing the importance of regional surveillance and antimicrobial stewardship to suggest effective treatment strategies. It is recommended that WGS of more strains be deposited to overcome limited data, and laboratory tests be performed to analyse the consistency between genetic predicted and phenotypic resistance.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110425"},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of different riboflavin concentrations and infiltration times on rabbit scleral crosslinking","authors":"Yuyan Huang ,&nbsp;Rongrong Gao ,&nbsp;Zheng Li ,&nbsp;Aodong Chen ,&nbsp;Qingqing Jiang ,&nbsp;Shengnan Ding ,&nbsp;Ming Chen ,&nbsp;Keith M. Meek ,&nbsp;Qinmei Wang ,&nbsp;Zhongxing Chen ,&nbsp;Jinhai Huang","doi":"10.1016/j.exer.2025.110449","DOIUrl":"10.1016/j.exer.2025.110449","url":null,"abstract":"<div><div>To explore the photosensitizer content, diffusion depth and crosslinking effects in rabbit sclera with different riboflavin (Rf) infiltration times and concentrations. For the fluorescence study, rabbit eyes were infiltrated in Rf solutions of different concentrations for different durations on the sclera. The scleral Rf infiltration depth and fluorescence intensity were analyzed with an LSM710 confocal microscope, and the Rf content was detected by the absorbance of the sclera homogenate supernatant. Ultraviolet A was used to perform scleral crosslinking (SXL). The effect of SXL was evaluated using uniaxial tensile testing and enzymatic resistance testing, and the biological safety was evaluated using HE and TUNEL staining. Transmission electron microscopy (TEM) observation was used to clarify the change in collagen fiber diameter. Rf quickly infiltrated the full scleral thickness at 0.05 % concentration for 5 min. The scleral Rf content was not statistically different after infiltration with 0.5 % Rf for 5 min or 10 min. The scleral tissues of the 0.1 % Rf-30 min group and the 0.5 % Rf-5 min group were digested completely within 22.7 ± 1.9 h and 25.3 ± 5.5 h, respectively. At 10 % strain, the Young's modulus of the 0.5 % Rf-5 min group was significantly higher than the control group (<em>P</em> = 0.0004). No obvious structural damage was observed in the retina or sclera, and the diameter of collagen fibers in the outer and middle scleral layers increased significantly after SXL. Ultimately, Rf infiltration at a concentration of 0.5 % for 5 min helped to shorten operation time and improve SXL effects.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110449"},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of pigment epithelium-derived factor and associated peptides on the differentiation of retinal ganglion cells from human-induced pluripotent stem cells","authors":"Chao-Wen Lin ,&nbsp;Shang-Chih Yang ,&nbsp;Vladlen Klochkov ,&nbsp;Ta-Ching Chen ,&nbsp;Wei-Kai Huang ,&nbsp;Wei-Li Chen","doi":"10.1016/j.exer.2025.110440","DOIUrl":"10.1016/j.exer.2025.110440","url":null,"abstract":"<div><div>Retinal ganglion cell degeneration is the main cause of irreversible vision loss in optic neuropathies. Pigment epithelium-derived factor (PEDF) and its smaller peptide components (44-mer and 17-mer) have shown neuroprotective effects. In this study, using a stepwise protocol we investigated their effects on human-induced pluripotent stem cell differentiation to retinal ganglion cells. Various concentrations of PEDF, 44-mer and 17-mer were added at day 18. Investigated compounds significantly upregulated the expression of retinal ganglion cells-specific (Brn3b, Sncg), retinal progenitor (Pax6) and neuroaxonal markers (Tau, NFH). They also highly increased Brn3b expression, as well as neurite length and density, supporting their neurotrophic properties. Our findings suggest that PEDF and its smaller peptide components, 44-mer and 17-mer, can be suggested as neuroprotective agents for the promotion of retinal ganglion cell differentiation from human-induced pluripotent stem cells. 44-mer and 17-mer have comparable or even higher effects to full-length PEDF and might also bypass PEDF usage limitations.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110440"},"PeriodicalIF":3.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting mitochondrial dysfunction: Innovative strategies to combat glaucoma neuroinflammation","authors":"Wen Lu ,&nbsp;Zhimin Liao ,&nbsp;Xinchen Jiang ,&nbsp;Manjuan Peng ,&nbsp;Que Deng ,&nbsp;Xiaoyu Zhou ,&nbsp;Ming Lu ,&nbsp;Xuanchu Duan","doi":"10.1016/j.exer.2025.110441","DOIUrl":"10.1016/j.exer.2025.110441","url":null,"abstract":"<div><div>Glaucomatous optic neuropathy represents a prevalent optic nerve degenerative disease. Neuroinflammation is recognized as a significant mechanism underlying optic nerve damage in glaucoma; however, the precise mechanisms driving neuroinflammation remain largely elusive. Existing studies have indicated that microglia-driven neuroinflammation is pivotal for neuroinflammation onset and progression. Mitochondrial dysfunction, encompassing mitochondrial DNA (mtDNA) damage, metabolic deficiencies, and quality control impairments, is upstream of microglial activation and neuroinflammation. Thus, a deeper comprehension of the link between mitochondrial dysfunction and microglial activation in glaucoma may provide valuable insights into the underlying pathogenesis. As a result of these findings, promising avenues for developing effective interventions to mitigate optic nerve damage and preserve visual function in glaucoma patients have been identified.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110441"},"PeriodicalIF":3.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M2 Macrophages Mitigate Ocular Surface Inflammation and Promote Recovery in a Mouse Model of Dry Eye.","authors":"Wang Yingming, Gao Jing, Wu Tianhong, Wang Zhenyu","doi":"10.1016/j.exer.2025.110439","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110439","url":null,"abstract":"<p><p>Dry eye disease (DED) is a chronic, progressive, multifactorial condition characterized by tear film instability and ocular surface damage. Ocular surface inflammation, triggered by multiple pathogenic factors, represents one of the key mechanisms in DED pathogenesis. This study aims to investigate the therapeutic effects of anti-inflammatory M2 macrophages conditioned medium (M2-CM) on ocular surface inflammation and their potential mechanisms in improving dry eye symptoms in a mouse model. Mouse macrophages (RAW264.7) were polarized into M2 macrophages by IL-4 under different osmolarities, and M2-CM was collected. Flow cytometry and ELISA were applied to measure the cytokine expression of the M2 macrophages. Primary mouse corneal epithelial cells (CECs) were co-cultured with RAW264.7 and M2 macrophages using a Transwell system. The viability and migration of CECs were assessed using CCK-8 and scratch assays. Mouse DED was established by subcutaneous injection of scopolamine, and the therapeutic effects of M2-CM were evaluated by phenol red thread test, fluorescein staining, and tear film breakup time (TBUT). PCR and immunofluorescence staining were applied to observe inflammatory factors and cells on the ocular surface. M2 macrophages enhanced CEC viability, proliferation, and migration, but hyperosmolarity inhibited M2 macrophage polarization. In the DED model, M2-CM improved ocular surface conditions, reduced pro-inflammatory cytokine expression, and increased anti-inflammatory factors. Immunofluorescence revealed reduced pro-inflammatory cells (M1 macrophages, Th1, and Th17) and increased M2 macrophages in the ocular tissues after M2-CM treatment. These results suggest that M2-CM ameliorates ocular surface inflammation and promotes recovery in DED, offering a potential therapeutic strategy for DED.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110439"},"PeriodicalIF":3.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}