Experimental eye research最新文献

{"title":"Cathepsin H deficiency leads to myopic phenotype in mice","authors":"Hao Mou ,&nbsp;Haicheng She ,&nbsp;Chang-Jun Zhang ,&nbsp;Min Li ,&nbsp;Wen Wang ,&nbsp;Shu-Ning Sun ,&nbsp;Xiao Zhang ,&nbsp;Zi-Bing Jin","doi":"10.1016/j.exer.2025.110447","DOIUrl":"10.1016/j.exer.2025.110447","url":null,"abstract":"<div><div>Genetic predisposition has been increasingly reported in patients with high myopia. A previous study reported that a deleterious mutation in cathepsin H (<em>CTSH</em>) gene causes high myopia. However, the phenotypic and mechanistic characteristics of <em>Ctsh</em>-deficient mice remain unknown. In this study, we generated a <em>Ctsh</em> knockout mouse model using CRISPR/Cas9, and confirmed the abolishment of <em>Ctsh</em> by Sanger sequencing. In the mouse model, myopic shift was measured by photorefraction and axial elongation was detected by magnetic resonance imaging (MRI). Retinal function detected by electroretinogram (ERG) indicated the scotopic responses of knockout mice were reduced, and slight retinal thinning was observed using optical coherence tomography (OCT). In addition, ribonucleic acid sequencing (RNA-seq) and real-time polymerase chain reaction (RT-PCR) demonstrated gene expression changes in the retinas of knockout mice. Our results indicated that <em>Ctsh</em> plays an important role in emmetropization and that its loss-of-function leads to myopia development.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110447"},"PeriodicalIF":3.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186878","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":"Smartphone-based fundus imaging and computer vision analysis for monitoring retinopathy of prematurity in neonatal rats with and without lutein treatment","authors":"Nolan McKibben ,&nbsp;Yanqi Zhang ,&nbsp;Shenglin Li ,&nbsp;Lingyan Kong ,&nbsp;Libo Tan","doi":"10.1016/j.exer.2025.110460","DOIUrl":"10.1016/j.exer.2025.110460","url":null,"abstract":"<div><div>Retinopathy of prematurity (ROP), caused by oxidative stress leading to abnormal retinal vessel growth, is often studied in rodent models. However, current methods rely on <em>in vitro</em> analysis, preventing the monitoring of disease progression. Fundus imaging is commonly used in clinical ophthalmology and could provide a method for <em>in vivo</em> imaging in rodents with ROP. Recently, a smartphone and condensing lens have been shown to be effective in humans and mice. The aim of this study was to develop a smartphone-based fundus camera system that can be used to monitor <em>in vivo</em> changes caused by ROP and determine its effectiveness upon introducing an intervention of lutein. KRN 633 was used to induce ROP and fundus imaging was conducted using a condensing lens and a smartphone. <em>In vitro</em> analysis of the retina was conducted for comparison using immunohistochemistry. The tortuosity was analyzed from fundus images manually using ImageJ and by a newly developed computer vision-based method. ROP induced tortuous arteries, which was improved by the administration of lutein in the fundus and microscopy images of the retina. The two imaging techniques showed a strong positive correlation. Similarly, the computer vision-based tortuosity analysis displayed a strong linear relationship with ImageJ analysis. This smartphone-based fundus camera system offers a cheap and accessible method for <em>in vivo</em> imaging to supplement traditional histological analysis. With future development, the image processing technique described can be enhanced to include other measures of visual function.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110460"},"PeriodicalIF":3.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186879","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":"Binocular dysfunction in Parkinson's Disease: Decoding near triad dynamics and divergence deficits","authors":"Pooja Nambiar ,&nbsp;Aasef G. Shaikh ,&nbsp;Palak Gupta ,&nbsp;Jordan Murray ,&nbsp;Fatema F. Ghasia","doi":"10.1016/j.exer.2025.110458","DOIUrl":"10.1016/j.exer.2025.110458","url":null,"abstract":"<div><div>Parkinson's Disease (PD) is a progressive neurodegenerative disorder that often affects the oculomotor system, causing strabismus and vergence impairments, particularly convergence insufficiency when focusing on nearby objects. This study evaluated eye deviation, vergence, accommodation, and pupil responses in PD during converging and diverging gaze shifts, correlating these findings with neurologic severity using the Unified Parkinson's Disease Rating Scale (UPDRS). We recruited 19 participants with varying severity of PD and 10 age-matched controls. 26 % of PD participants (PD Group 1) exhibited disparity-driven convergence and divergence responses comparable to controls, with expected miosis during convergence and mydriasis during divergence. In contrast, 74 % of PD participants (PD Group 2) showed reduced disparity-driven convergence and divergence, with diminished miosis during convergence and mydriasis during divergence. 37 % of PD participants exhibited increased exodeviation at near (30 cm) during binocular viewing in addition to reduced disparity-driven convergence. Blur-driven vergence was more significantly reduced than disparity-driven vergence in both PD participants and controls, likely due to presbyopia. Accommodation, assessed through changes in refractive error during disparity-driven and blur-driven vergence movements, was comparable between controls and PD patients. Our study indicates that PD disrupts disparity-driven convergence and divergence while sparing accommodation and blur-driven vergence. These findings offer insight into the pathophysiology of binocular dysfunction in PD, highlighting the involvement of neural structures such as the deep cerebellar nuclei and the supra-oculomotor area in vergence deficits and strabismus. Future studies can use these metrics to evaluate the effectiveness of targeted neuromodulation therapies in alleviating binocular dysfunction in PD.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110458"},"PeriodicalIF":3.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144178477","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":"NLRP3 proteins translocation into nuclei mediates SV40 T-antigen-induced corneal epithelial cell immortalization","authors":"Jie Xu ,&nbsp;Changkai Jia ,&nbsp;Qiaocheng Qiu ,&nbsp;Yuzhen Qin ,&nbsp;Yuting Wang ,&nbsp;Sijin Wu ,&nbsp;Wei Li ,&nbsp;Shengwei Ren ,&nbsp;Yiqiang Wang","doi":"10.1016/j.exer.2025.110455","DOIUrl":"10.1016/j.exer.2025.110455","url":null,"abstract":"<div><div>NLRP3 proteins mainly act as inflammasome core components in cytosol, but was sparsely recorded to translocate into nuclei in some conditions, such as in human simplex virus (HSV)-infected corneas, in SV40 T-Ag-immortalized human corneal epithelial cell (HCEC) line, or during differentiation of naïve T cells. This study was designed to define whether or how SV40 T-Ag transfection <em>per se</em> caused NLRP3 translocation. It was demonstrated that infection of primary human corneal epithelial cells with lentivirus coding for SV40 T-Ag induced NLRP3 proteins' translocation into nuclei. Pull-down of NLRP3-containing complexes in HCEC nuclear proteins followed by mass spectrometry revealed 285 nuclear proteins interacting with NLRP3 proteins. Clustering analysis of these proteins showed that “RNA binding”, “Nucleocytoplasmic transport” and “Viral carcinogenic pathway” were among the enriched molecular function terms or KEGG pathways. Structural modeling showed significant but differential affinities between NLRP3 proteins and histone subunits. Systemic Evolution of Ligands by EXponential enrichment (SELEX) was utilized to define DNA motifs potentially bound by NLRP3 proteins <em>in vitro</em>, and in-depth analysis of SELEXed motifs confirmed that the genes harboring those motifs were significantly associated with transcription and RNA processing. This study demonstrated that during the process of SV40 T-Ag-mediated corneal cell immortalization, NLRP3 proteins translocated into nuclei and behaved like a transcription factor. Besides confirming NLRP3 proteins’ novel functions in non-immune cells or tissues like cornea, these findings also shed light on the mechanisms of virus-mediated immortalization or viral induced carcinogenesis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110455"},"PeriodicalIF":3.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181248","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":"Multi-omics analysis reveals lipid metabolism profiles and regulatory networks in meibomian glands aging","authors":"Chen Pengjie,&nbsp;Sun Yiming,&nbsp;Wu Han,&nbsp;Miao Qi,&nbsp;Xu Mingyu,&nbsp;Wang Jiawei,&nbsp;Xu Peifang,&nbsp;Ye Juan","doi":"10.1016/j.exer.2025.110457","DOIUrl":"10.1016/j.exer.2025.110457","url":null,"abstract":"<div><div>Aging is a significant risk factor for ocular surface diseases like meibomian gland dysfunction (MGD), which compromises tear film stability, leading to discomforts, visual impairment, and ocular structural damage. This study aims to elucidate the age-related changes in lipid metabolism and the regulation networks, providing insights into early pathogenic mechanisms and identifying potential molecular targets for preventing age-driven pathology in the MGs. We analyzed MGs from young (2 months) and aged (12 months) C57BL/6 mice using a multi-omics approach, transcriptomic analysis and lipidomic analysis. Our findings revealed shifts in lipid composition in aged MGs, especially with reduced phospholipid levels and elevated triglyceride (TG) levels. Differentially expressed genes (DEGs) in lipid metabolism were also identified, including glycerolipid, glycerophospholipid, and sphingolipid metabolism, forming a complex regulatory network of lipid metabolism. Some critical DEGs were validated by qPCR, confirming the upregulation of Akr1b8 (glycerolipid metabolism) and the downregulation of Mboat2 (glycerophospholipid metabolism), Degs2, and Sptlc3 (sphingolipid metabolism) in aged MGs. These findings highlighted lipid metabolism dysregulation as a key factor in age-related MGD, offering potential targets for future research to mitigate this condition and preserve ocular health.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110457"},"PeriodicalIF":3.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180100","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":"Breaking barriers in ocular drug delivery for Uveitis: Advanced drug delivery systems, challenges and future prospects","authors":"Anju Ambekar,&nbsp;Jagannath Sahoo,&nbsp;Kavita Singh","doi":"10.1016/j.exer.2025.110456","DOIUrl":"10.1016/j.exer.2025.110456","url":null,"abstract":"<div><div>Uveitis is inflammation of the uvea, the middle layer of the eye which comprises of iris, ciliary body and choroid. Complications associated with uveitis include chronic pain, vision impairment and even blindness if not treated adequately. Conventional treatments for uveitis include immunosuppressive medications such as corticosteroids and biologics, which present challenges of low bioavailability due to complex anatomical structure of eye, rapid drug elimination, enzymatic degradation and the blood-retinal barrier. Consequently, they require frequent administration and are often associated with systemic side effects. In comparison to conventional drug delivery advanced drug delivery systems offer advantages such as targeted drug delivery, sustained drug release and reduction in side effects. A thorough literature search was conducted using Google Scholar, PubMed, covering publications from 2000 to 2024. The search terms included “uveitis,” “pathology and pathophysiology of uveitis,” “barriers in ocular drug delivery,” and “uveitis conventional treatments.” To refine the search results, “uveitis” was combined with different keywords such as “polymeric nanoparticles,” “liposomes,” “nanomicelles,” “dendrimers,” “nanoemulsions,” “hydrogels,” “implants,” or “microneedles” to gather information related to each novel drug delivery system. Only English language studies were considered. The inclusion criteria encompassed both review and research articles specifically related to uveitis, with a focus on studies evaluating novel drug delivery systems for its treatment. Studies on ocular drug delivery systems unrelated to uveitis were excluded. No formal statistical analysis was conducted. This review highlights various advanced drug delivery approaches including polymeric nanoparticles, liposomes, nanomicelles, dendrimers, nanoemulsions, hydrogels, implants and microneedles for the treatment of uveitis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110456"},"PeriodicalIF":3.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166806","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":"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-containing nuclear protein in eye health and disease: A review","authors":"Wahab Hussain ,&nbsp;Zhi-Liang Jiang ,&nbsp;Yi Liu ,&nbsp;Jia-Yi Wang ,&nbsp;Talat Bilal Yasoob ,&nbsp;Syed Ashiq Hussain ,&nbsp;Umm E. Laila ,&nbsp;Dong-Dong Wu ,&nbsp;Xin-Ying Ji ,&nbsp;Ya-Long Dang","doi":"10.1016/j.exer.2025.110451","DOIUrl":"10.1016/j.exer.2025.110451","url":null,"abstract":"<div><div>The human visual system plays a crucial role in how we perceive the world. However, it is susceptible to ocular conditions that can result in visual impairments. Globally, over 2.2 billion people suffer from vision impairments, including macular degeneration, refractive errors, cataracts, and glaucoma. In the field of iridology and ocular biology, essential proteins governing ocular homeostasis are frequently mutated or dysregulated. Clear vision is essential for people, and mutations related to these proteins can significantly impact the prevalence and progression of eye disorders. This review discusses proteins linked to ocular disorders, including the nuclear protein Ras, the human ER1 protein, and the PEST-containing nuclear protein (PCNP). Identifying and studying potential therapeutic targets and strategies to regulate these proteins is crucial for minimizing the burden of eye disorders. PCNP has been specifically linked to the development of several eye disorders. An understanding of these molecular processes will facilitate the development of clinical strategies to treat ocular disorders effectively. The main focus of this review is PCNP because of its significant role in the pathophysiology of eye disorders. Dysregulation of this protein has been linked to several ocular diseases, highlighting the need to clarify its functions. A comprehensive understanding of these essential proteins is vital for developing effective treatments and preventive measures against ocular pathologies. This review aims to advance global research, treatment, and management of preventable blindness and vision impairment by exploring strategies to target and regulate these potential therapeutic candidates.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 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}