Experimental eye research最新文献

{"title":"Differential analysis of core complement components expression and localization across rodent, non-human primate, and human ocular tissues","authors":"Aarin Jones,&nbsp;Aixu Sun,&nbsp;Hua Yang,&nbsp;Adrianna Latuszek,&nbsp;Nicole Negron,&nbsp;Peisheng Shi,&nbsp;Wen Fury,&nbsp;Guillermo L. Lehmann,&nbsp;Ying Hu,&nbsp;Botir Sagdullaev","doi":"10.1016/j.exer.2025.110433","DOIUrl":"10.1016/j.exer.2025.110433","url":null,"abstract":"<div><div>Age-related macular degeneration (AMD) is a leading cause of blindness. Genetic and pathophysiological studies have implicated that complement pathway dysfunction is a key contributor to progressive vision loss in AMD. Though the association between complement and AMD is recognized, numerous anti-complement therapeutics that had been tested in rodent model systems had limited success in clinical trials. Understanding complement factor production and site of action in ocular pathophysiology is critical for the development of efficacious therapeutics. However, our limited understanding of how these aspects of complement biology vary across species restricts our ability to predict clinical outcomes from studies using animal models. Here, we integrated transcriptomic and immunohistochemical assays to understand the expression and localization of core complement components (complement factor H (FH), complement 3 (C3), and complement 5 (C5)) between ocular tissues of rodent, non-human primate, and human species. We found that complement distribution varied significantly across the studied species, with the most striking differences observed in the FH. While rodents expressed <em>Cfh,</em> an alternative pathway inhibitor, mainly in the RPE, <em>CFH</em> expression in primate eyes was primarily confined to the choroid. These differences were consistent at the protein level, with rodent FH localized in the RPE and primate FH within the choriocapillaris, choroid and sclera. Regarding C5, a terminal complement pathway component, we observed minimal ocular mRNA levels in all three species. However, we observed detectable protein levels in the RPE in rodents and the choroid in humans. Next, <em>C3</em> mRNA transcripts and C3 protein exhibited similar distribution in the choroid in both rodent and primate eyes. Together, our findings highlight key differences and similarities between rodent and primate complement biology that may offer insights into the translatability of animal models and inform the design of effective therapeutics.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110433"},"PeriodicalIF":3.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149993","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":"Susceptibility genes for allergic conjunctivitis revealed by cross-tissue transcriptome-wide association study","authors":"Qin Xu,&nbsp;Yiping Li,&nbsp;Xin Zhang","doi":"10.1016/j.exer.2025.110444","DOIUrl":"10.1016/j.exer.2025.110444","url":null,"abstract":"<div><div>Allergic conjunctivitis (AC) is a common immune-mediated ocular disorder, characterized by clinical manifestations such as ocular itching, conjunctival hyperemia, lacrimation, and mucoid discharge, which significantly impair patients' visual function and quality of life. Despite extensive research efforts devoted to uncovering the genetic predisposition to AC, the underlying pathogenic genes and molecular mechanisms remain incompletely understood, necessitating further research to elucidate its genetic basis. This study utilized AC data from the FinnGen R12 and incorporated expression quantitative trait loci data in the Genotype-Tissue Expression v8 database to perform a cross-tissue transcriptome-wide association study (TWAS). Analytical methods included functional summary-based imputation (FUSION), unified test for molecular signatures (UTMOST), and gene analysis combined with multi-marker genome annotation (MAGMA). To further validate the results, Mendelian randomization (MR) analysis and colocalization analysis were performed. Through TWAS and MAGMA analyses, 13 susceptibility genes associated with AC were identified. Following MR and colocalization analyses, three candidate genes—GAL3ST2, PDCD1 and TLR6—were ultimately selected and validated by FUMA tool, which may influence progression of AC by regulating pathways related to Toll-like receptor signaling. In conclusion, three susceptibility genes linked to the risk of AC were identified, providing new insights into the genetic mechanisms and potential pathogenic pathways underlying AC.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110444"},"PeriodicalIF":3.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139456","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":"TRPV1 attenuates epithelial-mesenchymal transition via calpain-protein tyrosine phosphatase pathway in lens epithelial cells","authors":"Yosuke Nakazawa ,&nbsp;Fuko Nishizawa ,&nbsp;Sara Kawata ,&nbsp;Yuki Sugiyama ,&nbsp;Noriaki Nagai ,&nbsp;Naoki Yamamoto ,&nbsp;Megumi Funakoshi-Tago","doi":"10.1016/j.exer.2025.110435","DOIUrl":"10.1016/j.exer.2025.110435","url":null,"abstract":"<div><div>TRPV1, which is widely expressed throughout the body, is a non-selective cation channel activated by capsaicin. We previously reported that TRPV1 activation suppressed TGFβ2-induced epithelial-mesenchymal transition (EMT) by inhibiting Epidermal Growth Factor Receptor (EGFR) phosphorylation in lens epithelial cells (Sugiyama et al., 2021). However, the detailed molecular mechanism remains unclear. In this study, we focused on the calpain–protein tyrosine phosphatase (PTP) pathway to elucidate the detailed mechanism underlying TRPV1-induced EMT suppression. Calpain and PTP inhibitors mitigated the suppressive effect of capsaicin on TGFβ2-induced EMT <em>in vitro</em> and <em>ex vivo</em>. Finally, we shown that CalpainS1 and PTPN9 overexpression abrogated the effect of capsaicin on EMT in lens epithelial cells. Our findings indicate that calpain and PTP proteins are good candidates for preventing EMT after cataract surgery.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110435"},"PeriodicalIF":3.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149994","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":"PEST Proteolysis Signals Containing Nuclear Protein Related Proteins in Eye and Eye Diseases:A Review.","authors":"Wahab Hussain, Zhi-Liang Jiang, Yi Liu, Jia-Yi Wang, Talat Bilal Yasoob, Syed Ashiq Hussain, Umm E Laila, Dong-Dong Wu, Xin-Ying Ji, Ya-Long Dang","doi":"10.1016/j.exer.2025.110451","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110451","url":null,"abstract":"<p><p>The human visual system is a critical component for understanding the world around us, but it is affected by various eye conditions that lead to visual impairments. More than 2.2 billion people worldwide suffer from vision problems such as macular degeneration, refractive errors, cataracts, and glaucoma. In the field of iridology, essential proteins for maintaining healthy eye activity are often mutated or dysregulated. Clear vision is essential for people, and mutations related to these proteins can significantly impact the prevalence and development of eye disorders. Proteins that are linked to ocular disorders, including the nuclear protein Ras, S-glutathionylation, the human ER1 protein, and the Pest Proteolysis Signal-containing Nuclear Protein (PCNP), were examined in this study. Identifying and studying potential treatment targets and strategies to regulate the function of these proteins is crucial for minimizing the prevalence of eye disorders. PCNP is specifically linked to the development of several eye disorders. The development of clinical strategies to effectively treat ocular disorders will benefit from an understanding of these molecular processes. The main focus of this study was on PCNP because of due to its significant role in the pathophysiology of eye disorders. Understanding the function of this protein is vital, as its dysregulation has been linked with several ocular diseases. It is important to fully understand the roles of these essential proteins to develop effective treatments and preventive measures for ocular problems. This review therefore aims to contribute to advancements in the research, treatment, and management of preventable blindness and vision impairment globally by influencing thoughts on how to target and regulate these prospective remedies.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110451"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142001","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":"Visualizing sphingomyelin in the retina","authors":"Cassandra Warden ,&nbsp;Dalton Raymond ,&nbsp;Alex Sanchez ,&nbsp;Mathew Seidel ,&nbsp;Michael L. Risner","doi":"10.1016/j.exer.2025.110446","DOIUrl":"10.1016/j.exer.2025.110446","url":null,"abstract":"<div><div>Sphingomyelin (SM) is a major component of cellular membranes that is altered by retinal and optic nerve degenerations. However, our understanding of the influence of SM during degenerations is hampered by methodological limitations. Prior investigations have demonstrated the accumulation of SM to plasma membranes of cultured cells, using an enhanced green fluorescent non-toxic truncated form of lysenin (EGFP-NT-Lys), which is a protein that specifically binds to SM. Here, we used EGFP-NT-Lys and a permeabilization-free method for immunohistochemistry, which preserves membrane integrity, to demonstrate the accumulation of SM to the plasma membranes of retinal ganglion cells (RGCs) and retinal endothelial cells (RECs) of the intact mouse retina. To determine the sensitivity and selectivity of EGFP-NT-Lys for SM and SM species, we performed lipid dot blot assays. We found EGFP-NT-Lys is highly selective for SM and preferentially binds to longer-chain SMs. We confirmed that EGFP-NT-Lys labeling of SM is modifiable by treatment with the catabolic enzyme, sphingomyelinase. In addition, we verified EGFP-NT-Lys binding to SM by competition assays and EGFP. Confocal image analysis of immunofluorescence of RGC and REC markers and EGFP-NT-Lys labeling in flat mount mouse retinas revealed SM heavily accumulates within the retinal vasculature and around the perimeter of RGCs. Our data demonstrates that EGFP-NT-Lys combined with a permeabilization-free method for immunohistochemistry can be used to detect and quantify plasma membrane associated SM in defined cells of the intact retina.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110446"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142012","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 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}