Investigative ophthalmology & visual science最新文献

{"title":"Does the Association Between Eye Disease and Cognitive Function Vary by Genetic Risk of Cognitive Decline? An Analysis of Hospital Data With Replication in the Canadian Longitudinal Study on Aging.","authors":"Emily Tran, Mohan Rakesh, Gisele Li, Ellen E Freeman, Marie-Hélène Roy-Gagnon","doi":"10.1167/iovs.66.6.71","DOIUrl":"10.1167/iovs.66.6.71","url":null,"abstract":"<p><strong>Purpose: </strong>Age-related eye diseases are inconsistently associated with cognitive decline which could be due to effect modification. The purpose of this study was to investigate whether two genetic factors previously found to be associated with cognitive decline, the KIBRA (WWC1) and PDE7A/MTFR1 genes, modify the association between eye disease and cognitive function.</p><p><strong>Methods: </strong>Data from a Montreal hospital-based cross-sectional study (n = 302) were used for the primary analysis. Candidate single-nucleotide polymorphisms (SNPs) rs17070145 (KIBRA gene) and rs10808746 (PDE7A/MTFR1 gene) were included in linear regression models to test for effect modification of the relationship between eye disease (glaucoma or age-related macular degeneration [AMD]) and cognitive function. Six oral cognitive tests were used. A replication analysis was done using the Quebec data from the Canadian Longitudinal Study on Aging (CLSA) (n = 4238). Effect modifications by expanded genomic regions around the candidate SNPs were tested.</p><p><strong>Results: </strong>Three statistically significant interactions with two cognitive function measures -category verbal fluency and immediate story recall-were found in the Montreal study: glaucoma and AMD with rs17070145 and verbal fluency (P < 0.03) and glaucoma with rs10808746 with immediate story recall (P < 0.05). Similar interactions, although not with the same cognitive measure, were found in the CLSA: AMD with KIBRA and glaucoma with PDE7A/MTFR1.</p><p><strong>Conclusions: </strong>Our results suggest that the KIBRA and PDE7A/MTFR1 genes may modify the association between eye disease and cognitive function. This knowledge may help to better understand the mechanism by which glaucoma and AMD are related to cognitive function.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"71"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12186830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-Dimensional Culture of Orbital Fibroblasts From Thyroid Eye Disease Induce In Vivo-Like Tissue Remodeling and Fibrosis.","authors":"Xiaoli Bao, Zhihui Xu, Xi Wang, Te Zhang, Huijing Ye, Huasheng Yang","doi":"10.1167/iovs.66.6.67","DOIUrl":"10.1167/iovs.66.6.67","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the characteristics and molecular mechanisms of orbital fibroblasts under three-dimensional (3D)-culture conditions.</p><p><strong>Methods: </strong>Orbital connective tissue was collected from patients with thyroid eye disease (TED) and normal controls. Primary fibroblasts were cultured and used to generate 3D microspheres via the hanging drop. These spheroids were cultured for nine days, followed by biomechanical testing, transmission electron microscopy (TEM), and RNA sequencing for transcriptomic analysis. Multiplex immunofluorescence staining was used to assess fibrosis markers, and quantitative PCR validated gene expression changes. TED and normal control (NC) tissues, as well as primary cultured fibroblasts, were also subjected to transcriptomic sequencing.</p><p><strong>Results: </strong>TED-3D microspheres exhibited enhanced contractility, denser fiber deposition, and a characteristic fibrous ring at the periphery. TEM revealed more extracellular matrix (ECM) deposition and stronger tissue remodeling in TED-3D. Fibrosis markers (α-SMA, COL1A1, FN1) increased significantly in TED-3D. Biomechanical testing showed higher stiffness in TED-3D compared to NC-3D. Transcriptomic analysis revealed significant differences, with genes involved in ECM remodeling and fibrosis pathways enriched in TED-3D. Transcriptomic comparison of TED-tissue, TED-2D, and TED-3D revealed that TED-3D is closer to tissue than TED-2D.</p><p><strong>Conclusions: </strong>The 3D culture of orbital fibroblasts from TED induces in vivo-like tissue remodeling and fibrosis features. Compared to traditional two-dimensional culture, the expression pattern of TED-3D is closer to tissue, making it a more effective model for studying the mechanisms of TED-related fibrosis.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"67"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12186838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RAGE Is Essential for Subretinal Fibrosis in Laser-Induced Choroidal Neovascularization: Therapeutic Implications.","authors":"Parameswaran G Sreekumar, Mi-Hyun Nam, Elise Hong, Ram Kannan, Ram H Nagaraj","doi":"10.1167/iovs.66.6.30","DOIUrl":"10.1167/iovs.66.6.30","url":null,"abstract":"<p><strong>Purpose: </strong>Subretinal fibrosis, a complication of neovascular age-related macular degeneration (nAMD), involves the epithelial-mesenchymal transition (EMT) of retinal pigment epithelium (RPE) cells as a contributing mechanism. The receptor for advanced glycation end products (RAGE) is a multiligand receptor implicated in fibrotic diseases, but its role in subretinal fibrosis has not been studied. This study investigated the role of RAGE in subretinal fibrosis.</p><p><strong>Methods: </strong>Subretinal fibrosis was induced in male RAGE-/- and wild-type (WT) mice via laser photocoagulation, and fibrosis lesion volume was assessed on day 35 using optical coherence tomography and immunostaining. In vitro, EMT was induced in primary human RPE cells with transforming growth factor-beta 2 (TGF-β2). The role of RAGE in EMT was studied in cells pretreated with RAGE antagonists (FPS-ZM1 or azeliragon), followed by cotreatment with TGF-β2 for 48 hours. Signaling studies were conducted by pretreatment with FPS-ZM1 for 2 hours, cotreatment with TGF-β2 for 60 minutes, and subsequent immunoblot analysis.</p><p><strong>Results: </strong>In RAGE-/- mice, subretinal fibrosis after laser-induced choroidal neovascularization was significantly reduced, with a smaller fibrosis volume, less inflammation, decreased activation of pSmad2, and reduced deposition of fibrotic markers (αSMA, collagen I) compared to WT mice. In vitro treatment with TGF-β2 in human RPE cells increased mitochondrial reactive oxygen species and upregulated EMT markers (αSMA, collagen I, and fibronectin), which were inhibited by cotreatment with FPS-ZM1 or azeliragon. FPS-ZM1 blocked TGF-β2-induced Smad2-dependent signaling and EMT without affecting the extracellular signal-regulated kinase (ERK) pathway.</p><p><strong>Conclusions: </strong>Our findings indicate that RAGE plays a role in RPE cell EMT in subretinal fibrosis and that RAGE antagonists attenuate this process, making RAGE a promising therapeutic target for subretinal fibrosis in nAMD.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"30"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Studies of All-trans Retinoic Acid Transport in the Eye.","authors":"Saptarshi Chatterjee, Ankana Roy, Jianshi Yu, Arthur Thomas Read, Melissa R Bentley-Ford, Machelle T Pardue, Maureen A Kane, M G Finn, C Ross Ethier","doi":"10.1167/iovs.66.6.84","DOIUrl":"https://doi.org/10.1167/iovs.66.6.84","url":null,"abstract":"<p><strong>Purpose: </strong>Myopia incidence is increasing globally. All-trans retinoic acid (atRA) is important in myopigenic retinoscleral signaling, motivating research on its ocular transport. However, atRA's weak autofluorescence limits its direct visualization in tissues. Further, atRA is hydrophobic and must bind to protein carriers for transport. We assessed a fluorescent analog of atRA (LightOx 14, CAS:198696-03-6, referred as \"floRA\"), as an experimentally accessible atRA surrogate by: (i) evaluating its binding to carrier proteins and (ii) visualizing its distribution in ocular tissues.</p><p><strong>Methods: </strong>Binding: We assessed atRA-carrier protein binding using fluorescence quenching assays with bovine serum albumin (BSA), high density lipoprotein (HDL), apolipoprotein A-I (Apo A-I), and retinol binding protein 4 (RBP4). Direct visualization: Wild-type C57BL/6J mice were euthanized, their eyes were enucleated, and wedges containing sclera and choroid were incubated for specific durations in 50 µM floRA + BSA. The wedge centers were cryo-sectioned and counterstained for nuclei. Fluorescent micrographs were acquired and analyzed using ImageJ software.</p><p><strong>Results: </strong>Association constants (Ka) for atRA and floRA binding to carrier proteins were similar and ranged from 2 to 13 × 105 M-1, indicating nonspecific binding. floRA could be visualized in the sclera and choroid, yet showed significant spatial heterogeneity (enhanced fluorescence often colocalizing with nuclei).</p><p><strong>Conclusions: </strong>floRA is a reasonable surrogate for atRA binding to BSA, HDL, Apo A-I, and RBP4. Considering these proteins' relative serum and extravascular abundances, and their similar binding affinity to atRA, we predict that serum albumin is an important atRA carrier. Use of floRA in whole tissue tracer studies shows promise but requires further refinement.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"84"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528011","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":"Erratum in: Ferroptosis Contributes to Retinal Ganglion Cell Loss in GLAST Knockout Mouse Model of Normal Tension Glaucoma.","authors":"","doi":"10.1167/iovs.66.6.44","DOIUrl":"10.1167/iovs.66.6.44","url":null,"abstract":"","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"44"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyroptosis Mediated by ROS/Caspase-3/GSDME Pathway in Aspergillus fumigatus-Induced Fungal Keratitis.","authors":"Jingze Kan, Shiqi Song, Mengzhu Liu, Qiang Xu, Jieun Lee, Jintao Sun, Shasha Xue, Xiaoyan Sun, Chengye Che","doi":"10.1167/iovs.66.6.52","DOIUrl":"10.1167/iovs.66.6.52","url":null,"abstract":"<p><strong>Purpose: </strong>Gasdermin E (GSDME), cleaved by (casp-3) activation, is known as a key executor in pyroptosis. However, its role in fungal keratitis (FK) remains unclear. Thus we analyzed the role of GSDME, as well as its signaling pathway in Aspergillus fumigatus (AF)-induced FK.</p><p><strong>Methods: </strong>We conducted experiments using a mouse model and human corneal epithelial cells. Initially, we infected mice with AF at various time intervals and examined the progression of FK lesions, selecting the time point with the most severe lesions. Next, we pre-treated the subjects with various cytokine inhibitors that may influence pyroptosis. We then assessed the development of FK lesions and the production of inflammatory cytokines using qRT-PCR, flow cytometry, transmission electron microscopy, as well as Western blotting.</p><p><strong>Results: </strong>The optimal stimulation time for corneal epithelial cells in mice and humans was determined to be three days and 12 hours, respectively. In both the mouse and corneal epithelial cell models, GSDME significantly mediated AF-induced pyroptosis downstream of the reactive oxygen species (ROS)/casp-3/GSDME pathway and greatly influenced the inflammatory process and keratitis in AF-induced FK.</p><p><strong>Conclusions: </strong>Overall, GSDME played a crucial role in pyroptosis during corneal inflammation. By modulating IL-1β release during pyroptosis, GSDME had a significant impact on the host immune response in FK. This process could be inhibited by blocking the ROS/casp-3/GSDME pathway, potentially offering a novel treatment option for reducing corneal opacity in FK.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"52"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the Editor: \"VEP Latency Delay Reflects Demyelination Beyond the Optic Nerve in the Cuprizone Model\".","authors":"Henrique Rocha Mendonça, Ana Carolina de Pádua, Saulo Augusto Alves da Cruz, Greice Nascimento Pires, Sheila Espírito-Santo","doi":"10.1167/iovs.66.6.27","DOIUrl":"10.1167/iovs.66.6.27","url":null,"abstract":"","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"27"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-VEGF Agents Clearance Through the Aqueous Outflow Pathway in a Rat Model.","authors":"Assaf Ben-Arzi, Itay Spector, Yariv Keshet, Orly Gal-Or, Irit Bahar, Assaf Dotan","doi":"10.1167/iovs.66.6.1","DOIUrl":"10.1167/iovs.66.6.1","url":null,"abstract":"<p><strong>Purpose: </strong>Sustained increase in intraocular pressure (IOP) following intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF) in the treatment of retinal disease has been theoretically attributed to aggregation of anti-VEGF in the iridocorneal angle. However, previous studies by our group showed full clearance of intravitreally injected bevacizumab, aflibercept, and ranibizumab. The objective of this study was to further analyze and compare the clearance of these anti-VEGF agents from the eye after a single injection in a rat model.</p><p><strong>Methods: </strong>Brown Norway rats received an intravitreal injection of 3 µl anti-VEGF at the standard concentration 3 days following induction of choroidal neovascularization. The eyes were processed at 0, 3, 6, 24, and 48 hours thereafter, and immunofluorescence was evaluated with confocal microscopy and 3D reconstruction analysis. The signal concentration was calculated, and the drug clearance rate was measured. The immunohistochemistry process was validated with negative and positive control groups.</p><p><strong>Results: </strong>The immunofluorescent signal was positive for all anti-VEGF agents at the trabecular meshwork, Schlemm's canal, and episcleral veins. Anti-VEGF immunostaining peaked immediately after injection and then decreased gradually to negligible at 48 hours (P < 0.05). All three agents demonstrated an identical pattern (P > 0.05). The clearance rate of anti-VEGF from the iridocorneal angle ranged between 98.68% and 99.87% at 48 hours.</p><p><strong>Conclusions: </strong>Bevacizumab, aflibercept, and ranibizumab cleared completely from the iridocorneal angle at 48 hours in the brown Norway rats following a single intravitreal injection and with similar a clearance rate. These findings support our earlier studies refuting the anti-VEGF aggregation hypothesis.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"1"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes.","authors":"Yangqi Zhao, Yi Dong, Qingqing Zheng, Yue Zhao, Yingjie Ni, Peijin Qiu, Chuannan Chen, Mengyue Xu, Chaoyang Hong, Ting Shen","doi":"10.1167/iovs.66.6.6","DOIUrl":"10.1167/iovs.66.6.6","url":null,"abstract":"<p><strong>Purpose: </strong>Fatty acid desaturase 1 (FADS1) is significantly and specifically upregulated following diabetic corneal injury. However, its role in diabetic keratopathy remains unclear. This study aimed to investigate the impact of FADS1 on wound healing and functional recovery of the diabetic corneal epithelium and explore its potential mechanisms.</p><p><strong>Methods: </strong>Using high-glucose-induced corneal epithelial cells and a streptozotocin-induced type 1 diabetic mouse model, FADS1 expression was suppressed via FADS1 small interfering RNA (siRNA). Cell migration was assessed using scratch and transwell assays. Wound healing and functional recovery of the corneal epithelium were evaluated using sodium fluorescein staining, anterior segment optical coherence tomography, hematoxylin and eosin staining, and immunofluorescence staining.</p><p><strong>Results: </strong>FADS1 knockdown promoted wound healing and functional recovery of the diabetic corneal epithelium both in vivo and in vitro. Suppression of FADS1 enhanced high-glucose-induced corneal epithelial cell migration, which was dependent on elevated levels of the upstream metabolite γ-linolenic acid. This effect was mediated through the activation of the mitogen-activated protein kinase signaling pathway and the accumulation of autophagosomes.</p><p><strong>Conclusions: </strong>After diabetic corneal epithelial injury, FADS1 expression is specifically upregulated. Knockdown of FADS1 promotes wound healing and functional recovery, suggesting a novel therapeutic strategy for diabetic keratopathy.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"6"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choroidal Hyperreflective Foci Represent a Common Finding Across Different Types of Macular Atrophy.","authors":"Lorena Ulla, Claudio Foti, Alessandro Arrigo, Maurizio Battaglia Parodi, Maria Vittoria Cicinelli, Paola Marolo, Elisabetta Miserocchi, Mario Peronetti, Francesco Bandello, Enrico Borrelli, Michele Reibaldi","doi":"10.1167/iovs.66.6.42","DOIUrl":"10.1167/iovs.66.6.42","url":null,"abstract":"<p><strong>Purpose: </strong>To evaluate the presence, distribution, and potential implications of choroidal hyperreflective foci (HRFs) across different types of macular atrophy and their relationship with the size of atrophic regions.</p><p><strong>Methods: </strong>This retrospective case series analyzed 95 eyes from 87 patients with macular atrophy caused by various conditions, including geographic atrophy due to age-related macular degeneration, pachychoroid disease, punctate inner choroidopathy, angioid streaks, and Stargardt disease. Structural optical coherence tomography (OCT) images were evaluated to identify HRFs in different choroidal layers. HRF counts were correlated with the size of macular atrophy and underlying conditions using multiple regression analysis.</p><p><strong>Results: </strong>HRFs were observed in all cases, with their number significantly associated with the size of macular atrophy (P < 0.001). The highest HRF counts were found in Stargardt disease, while the lowest were in pachychoroid disease. However, no association was identified between HRF quantity and specific disease type (P = 0.2). HRFs were primarily located in the choriocapillaris, Sattler's layer, and near Bruch's membrane but were absent within choroidal vessels.</p><p><strong>Conclusions: </strong>HRFs represent a common OCT finding in various disorders associated with macular atrophy. Their quantity correlates with atrophy size rather than disease type, suggesting they are likely normal choroidal components rendered visible by RPE loss. Future studies are warranted to elucidate their origin and potential implications for disease progression.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"42"},"PeriodicalIF":5.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}