Pub Date : 2026-01-03DOI: 10.1016/j.exer.2026.110847
Yutian Pu , Chunjing Tao , Barbara K. Pierscionek , Kehao Wang
This study investigates the influence of zonular anchorage position and loading mechanism on lens accommodation using finite element analysis. Axisymmetric models of the lens–zonule–ciliary body complex were developed, incorporating anterior, equatorial, and posterior zonular bundles. Four model variants were generated by varying anchorage position (near the pars plicata or pars plana) and loading mechanism (synchronous or asynchronous). Lens morphology, central optical power (COP) and zonular forces were analysed during simulated accommodation. The synchronous loading mechanism induced greater changes in posterior lens and nuclear radii of curvature and produced a wider range of accommodative change, while the asynchronous mechanism induced higher anterior surface steepening and peak central optical power but a smaller accommodative range. Zonular anchorage position slightly affected outcomes only in models with synchronous loading mechanism such that models with anchorage position near the pars plicata yielded greater changes in COP. A nonlinear relationship between central optical power and zonular force was consistently observed, suggesting an optimal range of zonular tension for maximizing lens performance. These findings indicate that zonular loading mechanism significantly influence lens shape and optical performance.
{"title":"Lens shape change is influenced by zonular anchorage and stretching mechanism","authors":"Yutian Pu , Chunjing Tao , Barbara K. Pierscionek , Kehao Wang","doi":"10.1016/j.exer.2026.110847","DOIUrl":"10.1016/j.exer.2026.110847","url":null,"abstract":"<div><div>This study investigates the influence of zonular anchorage position and loading mechanism on lens accommodation using finite element analysis. Axisymmetric models of the lens–zonule–ciliary body complex were developed, incorporating anterior, equatorial, and posterior zonular bundles. Four model variants were generated by varying anchorage position (near the pars plicata or pars plana) and loading mechanism (synchronous or asynchronous). Lens morphology, central optical power (COP) and zonular forces were analysed during simulated accommodation. The synchronous loading mechanism induced greater changes in posterior lens and nuclear radii of curvature and produced a wider range of accommodative change, while the asynchronous mechanism induced higher anterior surface steepening and peak central optical power but a smaller accommodative range. Zonular anchorage position slightly affected outcomes only in models with synchronous loading mechanism such that models with anchorage position near the pars plicata yielded greater changes in COP. A nonlinear relationship between central optical power and zonular force was consistently observed, suggesting an optimal range of zonular tension for maximizing lens performance. These findings indicate that zonular loading mechanism significantly influence lens shape and optical performance.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110847"},"PeriodicalIF":2.7,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899652","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}
Autoimmune-associated orbital inflammation refers to the inflammation of orbital tissues resulting from immune system dysregulation. Interleukin-17 (IL-17) plays a critical role in immune defense, tissue repair, inflammation, and tumor progression. Given its immunomodulatory functions, this study aimed to investigate whether single-nucleotide polymorphisms (SNPs) in IL17-related genes contribute to susceptibility and clinical manifestations of orbital autoimmune diseases.
A total of 60 patients with orbital autoimmune disease and 60 healthy controls were recruited. Candidate SNPs in IL17A, IL17F, IL17RA, and IL17RC were selected based on known hotspots, including 500 bp upstream and downstream flanking regions. Associations between SNPs and disease status, as well as clinical features such as pain, diplopia, conjunctival inflammation, and eyelid retraction, were analyzed using chi-square or Fisher's exact tests.
The analysis revealed that rs9791323 in the promoter region of the IL17A gene was significantly associated with disease susceptibility (p = 0.045) but not with specific clinical features. Other SNPs were found to correlate with distinct symptoms: in IL17A, rs3804513 was associated with pain (p = 0.012); rs3819024 and rs2275913 with diplopia (p = 0.007 and 0.028, respectively); and rs8193036 with both diplopia (p = 0.002) and eyelid retraction (p = 0.033). In IL17F, rs9463772 was associated with pain (p = 0.005), while rs4715290 and rs11465530 were linked to eyelid retraction (p = 0.014 and 0.030, respectively). Three SNPs in IL17RA—rs4819553, rs4819958, and rs4819554—were significantly associated with conjunctival inflammation (p = 0.012). The IL17RC SNP rs708567 was also related to eyelid retraction (p = 0.049).
In conclusion, rs9791323 in IL17A may contribute to disease susceptibility, while other IL17-related SNPs appear to influence specific clinical features. These findings highlight the potential role of IL17 gene variants in both the pathogenesis and phenotypic variability of autoimmune-associated orbital inflammation.
{"title":"IL17-related gene polymorphisms associated with orbital inflammatory diseases and their clinical features","authors":"Ding-Ping Chen , Wei-Tzu Lin , Fang-Ping Hsu , Yen-Chang Chu","doi":"10.1016/j.exer.2025.110838","DOIUrl":"10.1016/j.exer.2025.110838","url":null,"abstract":"<div><div>Autoimmune-associated orbital inflammation refers to the inflammation of orbital tissues resulting from immune system dysregulation. Interleukin-17 (IL-17) plays a critical role in immune defense, tissue repair, inflammation, and tumor progression. Given its immunomodulatory functions, this study aimed to investigate whether single-nucleotide polymorphisms (SNPs) in IL17-related genes contribute to susceptibility and clinical manifestations of orbital autoimmune diseases.</div><div>A total of 60 patients with orbital autoimmune disease and 60 healthy controls were recruited. Candidate SNPs in IL17A, IL17F, IL17RA, and IL17RC were selected based on known hotspots, including 500 bp upstream and downstream flanking regions. Associations between SNPs and disease status, as well as clinical features such as pain, diplopia, conjunctival inflammation, and eyelid retraction, were analyzed using chi-square or Fisher's exact tests.</div><div>The analysis revealed that rs9791323 in the promoter region of the IL17A gene was significantly associated with disease susceptibility (p = 0.045) but not with specific clinical features. Other SNPs were found to correlate with distinct symptoms: in IL17A, rs3804513 was associated with pain (p = 0.012); rs3819024 and rs2275913 with diplopia (p = 0.007 and 0.028, respectively); and rs8193036 with both diplopia (p = 0.002) and eyelid retraction (p = 0.033). In IL17F, rs9463772 was associated with pain (p = 0.005), while rs4715290 and rs11465530 were linked to eyelid retraction (p = 0.014 and 0.030, respectively). Three SNPs in IL17RA—rs4819553, rs4819958, and rs4819554—were significantly associated with conjunctival inflammation (p = 0.012). The IL17RC SNP rs708567 was also related to eyelid retraction (p = 0.049).</div><div>In conclusion, rs9791323 in IL17A may contribute to disease susceptibility, while other IL17-related SNPs appear to influence specific clinical features. These findings highlight the potential role of IL17 gene variants in both the pathogenesis and phenotypic variability of autoimmune-associated orbital inflammation.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110838"},"PeriodicalIF":2.7,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145905632","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}
Glaucoma is one of the major causes of irreversible blindness worldwide. The disease is characterized by the progressive loss of retinal ganglion cells (RGCs), and recent evidence supports a key role for oxidative stress in the pathogenesis. In this review, we systematically examine the mechanisms of oxidative stress in the pathogenesis of RGC injury, including impaired mitochondrial function, neuroinflammation, and complement system dysregulation, as well as increased intraocular pressure (IOP). We then evaluate currently available neuroprotective strategies targeting these pathways and highlight in particular direct antioxidant therapies and inhibition of specific enzymes in the oxidative stress pathways. We then discuss recent advances powered by new methods such as single-cell multi-omics. A notable gap exists between encouraging results in preclinical models and less success in clinical trials. This disconnect points to important new directions for future research.
{"title":"Oxidative stress in glaucomatous retinal ganglion cell injury: Mechanisms and neuroprotective strategies","authors":"Yanzhi Xu , Peiyao Yu , Yifan Xie , Junze Yang , Jianbo Wu , Ling Ling , Wei Zhou","doi":"10.1016/j.exer.2025.110837","DOIUrl":"10.1016/j.exer.2025.110837","url":null,"abstract":"<div><div>Glaucoma is one of the major causes of irreversible blindness worldwide. The disease is characterized by the progressive loss of retinal ganglion cells (RGCs), and recent evidence supports a key role for oxidative stress in the pathogenesis. In this review, we systematically examine the mechanisms of oxidative stress in the pathogenesis of RGC injury, including impaired mitochondrial function, neuroinflammation, and complement system dysregulation, as well as increased intraocular pressure (IOP). We then evaluate currently available neuroprotective strategies targeting these pathways and highlight in particular direct antioxidant therapies and inhibition of specific enzymes in the oxidative stress pathways. We then discuss recent advances powered by new methods such as single-cell multi-omics. A notable gap exists between encouraging results in preclinical models and less success in clinical trials. This disconnect points to important new directions for future research.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110837"},"PeriodicalIF":2.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899703","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}
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