Experimental eye research最新文献

{"title":"Study on the Protective Effects and Mechanisms of Atorvastatin in Retinal Ischemia-Reperfusion Injury in Mice","authors":"Ke Yin ,&nbsp;Xinyi Li ,&nbsp;Haomin Chen ,&nbsp;Yanxin Zhang ,&nbsp;Yifei Dang ,&nbsp;Yi Shi ,&nbsp;Lijie Dong ,&nbsp;Aihua Liu","doi":"10.1016/j.exer.2025.110686","DOIUrl":"10.1016/j.exer.2025.110686","url":null,"abstract":"<div><div>Retinal ischemia-reperfusion injury (RIRI) is a major cause of visual impairment, with limited effective treatment options. Atorvastatin (Ato), recognized for its pleiotropic effects, has demonstrated potential neuroprotective and vasculoprotective properties. This study aimed to evaluate the protective effects of Ato in a murine RIRI model and elucidate its underlying molecular mechanisms. An RIRI model was established via anterior chamber saline perfusion. Retinal ganglion cell (RGC) survival, superficial vascular density, morphology, and function were assessed, identifying 7 days post-injury as the optimal time point for model evaluation. Subsequent oral Ato administration significantly preserved RGCs, vascular density, and retinal function compared to the untreated RIRI group. Transcriptomic analysis identified insulin-like growth factor 1 (IGF1) as a key differentially expressed gene following Ato treatment. KEGG pathway enrichment analysis suggested IGF1 involvement in the Mitogen-Activated Protein Kinase (MAPK) signaling pathway. qRT-PCR, Western blotting, and immunofluorescence confirmed upregulated IGF1 expression in Ato-treated mice. These findings indicate that Ato may confer neurovascular protection against RIRI by sustaining IGF1/IGF1R expression, potentially engaging downstream MAPK pathways, thereby preserving retinal neurons, vascular integrity, and visual function.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"261 ","pages":"Article 110686"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257811","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 and Protective Genes in Diabetic Retinopathy: A Comprehensive Single-Cell RNA Sequencing Analysis.","authors":"Jingqiu Li, Xinyang Hu, Hui Zhang, Yuming Li, Feilong Zhou, Dan Li, Haibo Zhang, Siqi Fan, Bing Shen, Yong Wang","doi":"10.1016/j.exer.2025.110673","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110673","url":null,"abstract":"<p><p>Diabetes, an epidemic marked by increased blood glucose levels, is an endocrine disorder projected to impact 693 million individuals by 2045. The disease leads to significant morbidity and mortality primarily due to vascular complications, such as cardiovascular disease and diabetic kidney disease, imposing substantial economic burdens globally. Notably, type 2 diabetes (T2D) exhibits considerable heterogeneity in mechanisms and health outcomes. Recent advancements in clustering techniques have revealed clinically distinct subgroups of T2D, emphasizing the complexity of its complications influenced by both genetic and environmental factors. In our study, we utilized single-cell RNA sequencing (scRNA-seq) profiles from peripheral blood mononuclear cells of individuals with diabetes and diabetic retinopathy (DR) to elucidate the genetic underpinnings of this complication. We identified key genes associated with the susceptibility and severity of DR, establishing a diabetic retinal regulatory network. Notable findings include the role of Discoidin Domain Receptor 1 (DDR1) in promoting proinflammatory pathways, while genes such as TELO2, SNX30 and HLA-DRA appear to confer protective effects. Our investigation highlights the intricate balance between risk and protective factors in DR pathogenesis. Furthermore, molecular docking analyses identified potential therapeutic agents targeting these genes, suggesting new avenues for treatment. Overall, our results underscore the importance of understanding genetic influences on DR and propose a framework for future research and therapeutic strategies aimed at mitigating diabetic complications.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110673"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274383","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 association of ARR3 genetic polymorphisms with pathologic myopia in Northern Chinese population.","authors":"Wenna Gao, Min Zhang, Guangqi An, Fan Yang, Lin Li, Xuemin Jin, Liping Du","doi":"10.1016/j.exer.2025.110691","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110691","url":null,"abstract":"<p><strong>Purpose: </strong>The study is conducted to illustrate the relationship between the single nucleotide polymorphisms (SNPs) of ARR3 and pathologic myopia (PM) among the general public residing in Northern China.</p><p><strong>Methods: </strong>PM patients and the emmetropic controls were recruited in Northern China. The venous blood samples of subjects were collected, following which DNA were extracted. Seven SNPs of the ARR3 gene, including rs10449043, rs11094147, rs1572732, rs1768567, rs3818861, rs4844220, and rs5936872, were genotyped by the iPLEX Gold Genotyping Assay. The SHEsis platform was employed to evaluate linkage disequilibrium and haplotype blocks, and the SPSS software was used to assess correlations.</p><p><strong>Results: </strong>There were 575 PM patients and 742 age-matched controls being enrolled in the study. No statistical significance was identified on the relationship between ARR3 SNPs and PM. Results of subgroup analyses based on the degree of chorioretinal atrophy indicated that compared with the heterozygote TC in rs1768567, the homozygotes TT and CC significantly protected the aggravation of female PM from the tessellated fundus to the diffuse chorioretinal atrophy. Although there existed the strong linkage disequilibrium among tested SNPs, 4 major haplotypes of them were not related to the onset and severity of PM.</p><p><strong>Conclusions: </strong>The study has emphasized the significance of ARR3 SNPs in the progression of chorioretinal atrophy in female PM.</p><p><strong>Trial registration: </strong>The study was retrospectively registered in the clinicaltrials.gov (identifier: NCT06204211).</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110691"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274385","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":"Increased efficacy of accelerated corneal collagen crosslinking in rabbit ectasia models due to higher oxygen availability.","authors":"Chenyan Wang, Jie Hou, Pengfei Han, Peng Chen, Junchao Wei, Hongwei Qin, Xiaona Li, Weiyi Chen","doi":"10.1016/j.exer.2025.110684","DOIUrl":"10.1016/j.exer.2025.110684","url":null,"abstract":"<p><p>The purpose of this study was to comprehensively investigate the efficacy and safety of accelerated corneal collagen crosslinking (A-CXL) in a normoxic or hyperoxic environment. The collagenase type Ⅱ solution was applied to both the left and right eyes of the rabbit after epithelial debridement. Two weeks after collagenase treatment, the corneal morphology parameters (by Pentacam) and biomechanical parameters (by Corvis ST) in vivo were assessed to determine whether corneal ectasia had occurred. Subsequently, these eyes were randomly divided into three groups. The first group did not receive any treatment. The second and third groups underwent A-CXL surgery (30 mW/cm², 4 min) in normoxic environment (21 % oxygen) or hyperoxic environment (>90 % oxygen), respectively. Four weeks later, changes in the corneal morphology parameters and biomechanical parameters in vivo were evaluated. Moreover, the elastic modulus (by biaxial stretch test) and histology of corneal tissues were also assessed ex vivo. Morphological and biomechanical parameters in vivo suggest the occurrence of corneal ectasia after collagenase treatment. No significant differences were found in morphological parameters changes obtained by Pentacam among three groups at 4 weeks after A-CXL surgery. However, the results of SD-OCT revealed that the corneal thickness change at the peripheral position along the nasal-temporal direction in the hyperoxic A-CXL group was lower compared with the other two groups. Biomechanical tests showed that, compared with the ectatic cornea group, the ability of the cornea to resist deformation increased only in the hyperoxic A-CXL group, with lower A1V and IR in vivo and higher elastic modulus ex vivo, while the normoxic A-CXL exhibited similar postoperative outcomes to untreated ectatic cornea. The histological results showed that no obvious signs of apoptosis were observed in all groups. In conclusion, hyperoxic A-CXL may be more effective than normoxic A-CXL in the aspect of delaying further cornea ectasia. This confirms the positive role of oxygen application in A-CXL in keratoconus clinic treatment.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110684"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257803","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":"Impact of Innate Immune Factors on the Persistence of Staphylococcus aureus in the Ocular Environment.","authors":"Michelle C Callegan, Md Mursalin Huzzatul, Luis Longoria-Gonzalez, Roger Astley, Phillip S Coburn","doi":"10.1016/j.exer.2025.110682","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110682","url":null,"abstract":"<p><p>Microbial keratitis can be detrimental to vision, causing corneal damage and inflammation that can lead to painful epithelial defects and scarring. Staphylococcus aureus is frequently isolated from bacterial keratitis cases. This organism's virulome and propensity for antibiotic resistance make it a formidable ocular pathogen that is often difficult to eradicate. S. aureus is not typically isolated from an immunocompetent ocular environment. We therefore hypothesized that elements of innate immunity are important in protecting the cornea from S. aureus infection, so their absence would facilitate persistence that might lead to keratitis. In the current study, we used a corneal scratch and topical inoculation model with S. aureus strain 8325-4 to infect mouse eyes and assess infection and inflammation in wild type C57BL/6J mice and mice genetically deficient in TLR2 (i.e. TLR2-/- or TLR2/4-/-) or TLR2-associated proinflammatory mediators (CXCL1-/-, CXCL2-/-, CXCL10-/-, CCL2-/-, CCL3-/-, or TNFα-/-). We included males and females in these experiments to determine whether sex was a biological variable. We assessed staphylococcal burden and clearance by quantifying colony forming units (CFU)/eye, inflammation by quantifying myeloperoxidase (MPO) from infiltrating neutrophils, and ocular pathology each day for 3-6 days, depending on the assay. Our data shows that, in general, the absence of the TLR2 pathway and its downstream mediators facilitated persistence of S. aureus in the mouse eye, but did not lead to ulcerative keratitis. S. aureus was cleared from the C57BL/6J mouse cornea within 3 days, while the organism persisted in knockout mouse eyes through day 6. Although pockets of staphylococci and neutrophil influx at the sites of infection were observed in some eyes, there were surprisingly very few corneal epithelial defects noted irrespective of mouse strain. These results suggest that defects in innate immunity create an environment that can facilitate persistence of S. aureus at the ocular surface, an area typically devoid of harmful bacteria.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110682"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274374","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":"Associations of PEDF Genetic Polymorphisms with Retinopathy of Prematurity.","authors":"Pei-Liang Wu, Eugene Yu-Chuan Kang, Xiao Chun Ling, Chia-Wen Lee, Kuan-Jen Chen, Nan-Kai Wang, Laura Liu, Yih-Shiou Hwang, Chi-Chun Lai, Shun-Fa Yang, Wei-Chi Wu","doi":"10.1016/j.exer.2025.110681","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110681","url":null,"abstract":"<p><p>The current study explores the association between pigment epithelium-derived factor (PEDF) polymorphisms and risk, severity, susceptibility, and treatment response of retinopathy of prematurity (ROP). The study is designed in a prospective cohort manner, where all participating patients were recruited from two hospital branches. Three single nucleotide polymorphisms of PEDF with the highest allele frequency were selected. The genomic data were extracted from the patient's blood and amplified using polymerase chain reaction (PCR). A multivariate logistic regression model assessed the association between PEDF polymorphisms and ROP risk. Risk evaluation for each polymorphism was performed using an adjusted odds ratio (OR). 51% of the 585 recruited patients developed ROP, subdivided into groups of type-2 or milder ROP and type-1 ROP. The results showed that patients with polymorphic genotype GA and the combination of genotypes GA and AA in the polymorphism of rs11658342 were associated with a higher risk of developing both type-2 or milder ROP (aOR = 1.757, p = 0.037; OR = 1.370, p = 0.013) and type-1 ROP (OR = 1.950, p = 0.013; OR = 1.358, p = 0.017). Patients with the polymorphic AA genotype in the polymorphism of rs12603825 had a higher risk of type-1 ROP (OR = 2.740, p = 0.029). The results indicate that patients with GA and AA genotypes in rs11658342 and rs12603825 of the PEDF polymorphism may serve as prognostic factors for ROP risks and severity.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110681"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274392","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":"Galectin-1 Overexpression Protects Damaged Optic Nerve and Visual Function in Mice by Inhibiting the p38/ MAPK-NF-κB Signaling Pathway.","authors":"Xuejun He, Ning Yang, Ningzhi Zhang, Wenye Cao, Lu Yu, Wenxi Zhang, Lan Yu, Yiqiao Xing","doi":"10.1016/j.exer.2025.110689","DOIUrl":"https://doi.org/10.1016/j.exer.2025.110689","url":null,"abstract":"<p><p>The role of galectin-1 (Gal-1) in traumatic optic neuropathy (TON) remains unclear. Therefore, we investigated the role and action mechanism of Gal-1 in TON induced by optic nerve crush (ONC). Forty male C57BL/6J mice were randomly divided into five groups: control (Con), ONC, phosphate-buffered saline (PBS) intravitreal injection, PBS intravitreal injection combined with ONC (PBS+ONC), and Gal-1 overexpression combined with ONC (Gal-1+ONC) groups. The PBS+ONC group was intravitreally injected with PBS and the Gal-1+ONC group was intravitreally injected with a recombinant adeno-associated virus carrying the Gal-1 target gene (TON was induced 23 days later). Subsequent experiments were performed 5 days post-ONC induction. Gal-1 expression was detected using western blotting (WB) and immunohistochemistry. Retinal ganglion cell (RGC) survival was examined using retinal flat mount immunofluorescence. Flash electroretinography and optomotor response analysis were used to determine retinal and visual functions. Furthermore, WB was performed to evaluate Gal-1-associated molecular mechanisms during TON. RGC survival rate and retinal and visual functions of mice decreased post-TON. However, Gal-1 overexpression inhibited ONC-induced RGC death, flash electroretinogram a-wave and b-wave amplitude decrease, and visual function decline. Moreover, p38/mitogen-activated protein kinase and nuclear factor-κB expression reduced with Gal-1 upregulation. Gal-1 exerts a protective effect against TON in mice by inhibiting the inflammatory response.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110689"},"PeriodicalIF":2.7,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274340","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":"circ-0007006 attenuates fibrosis in thyroid-associated ophthalmopathy by stabilizing HBEGF expression in vitro","authors":"Zhihui Xu ,&nbsp;Xiaoli Bao ,&nbsp;Anqi Sun,&nbsp;Lu Shi,&nbsp;Xi Wang,&nbsp;Yiwen Zeng,&nbsp;Hongru Chen,&nbsp;Te Zhang,&nbsp;Huasheng Yang ,&nbsp;Huijing Ye","doi":"10.1016/j.exer.2025.110683","DOIUrl":"10.1016/j.exer.2025.110683","url":null,"abstract":"<div><div>Thyroid-associated ophthalmopathy (TAO) is an autoimmune orbital disease characterized by inflammation and tissue remodeling, with fibrosis being a predominant and often irreversible feature in type II TAO. While immunosuppressive therapies offer limited efficacy, there remains a critical need to identify effective molecular targets for fibrotic TAO. Circular RNAs (circRNAs) have emerged as key regulators in various diseases, yet their roles in TAO are largely unexplored. In this study, we identified hsa_circ_0007006 as significantly downregulated in fibrotic TAO tissues through high-throughput RNA sequencing. Functional assays in orbital fibroblasts revealed that circ-0007006 suppresses fibrosis by downregulating COL1A1, α-SMA, HAS1, and HAS2, and inhibiting SMAD2/3 phosphorylation. Mechanistically, circ-0007006 functions as a competing endogenous RNA for miR-383-3p, thereby stabilizing HBEGF expression. Rescue experiments showed that exogenous HBEGF alleviates the pro-fibrotic effects induced by circ-0007006 knockdown. These findings identify the circ-0007006/miR-383-3p/HBEGF axis as a novel regulatory pathway in TAO fibrosis and support circ-0007006 as a potential therapeutic target for the fibrotic subtype of TAO.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"261 ","pages":"Article 110683"},"PeriodicalIF":2.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250289","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":"Polydatin's neuroprotective mechanism in optic nerve injury: targeting mitochondrial function and glial cell activation","authors":"Baoqi Hu ,&nbsp;Xin Wang ,&nbsp;Xiou Wang ,&nbsp;Sijia Zhou ,&nbsp;Yongtai Yan ,&nbsp;Jing Yang ,&nbsp;Bo Ma ,&nbsp;Qianyan Kang ,&nbsp;Zhichao Zhang ,&nbsp;Rui Wang","doi":"10.1016/j.exer.2025.110685","DOIUrl":"10.1016/j.exer.2025.110685","url":null,"abstract":"<div><div>Optic nerve injury (ONI) frequently causes irreversible visual impairment, making it a significant clinical challenge. This study evaluated the neuroprotective effects of polydatin (PD), focusing on its ability to preserve mitochondrial function and inhibit glial cell activation. We utilized an <em>in vitro</em> retina-ON explant culture model and a mouse ON crush (ONC) model. PD was administered to assess its impact on mitochondrial protection, apoptosis of retinal ganglion cells (RGCs), glial cell activation, and glial inflammatory responses. Western blot and immunofluorescence analysis were employed to examine the p38 MAPK signaling pathway. A primary retinal progenitor cells (RPCs) oxygen-glucose deprivation/reoxygenation (OGD/R) model was established to evaluate the direct protective effect of PD on retinal neuronal mitochondria. PD treatment significantly preserved mitochondrial numbers, reduced glial cell activation and inflammation, and decreased apoptosis of RGCs in the explant culture model. Western blot and immunofluorescence analysis confirmed the inhibition of the p38 MAPK signaling pathway, which is essential for glial cell activation. In the primary RPCs OGD/R model, PD enhanced cell viability, decreased apoptosis, and preserved mitochondrial integrity, demonstrating its direct protective effect on retinal neuronal mitochondria. These findings were further validated in the mouse ONC model, where PD reduced RGC loss, inflammation, and apoptosis. PD exhibits neuroprotective properties in models of retinal and ONI, likely through its dual mechanism of preserving mitochondrial function and inhibiting glial cell activation. These results support the potential therapeutic use of PD in treating conditions that lead to ON damage and RGC degeneration.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"261 ","pages":"Article 110685"},"PeriodicalIF":2.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250317","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":"Response to “Comment on “Structural changes in retinal and choroidal vasculature following N-methyl-N-nitrosourea-induced retinal degeneration in rats” by Shimoda et al.”","authors":"Kazuaki Shimoda,&nbsp;Mone Matsumoto,&nbsp;Akane Morita,&nbsp;Tsutomu Nakahara","doi":"10.1016/j.exer.2025.110679","DOIUrl":"10.1016/j.exer.2025.110679","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"261 ","pages":"Article 110679"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145217874","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}