Experimental eye research最新文献

{"title":"In vivo analysis of age-related changes in longitudinal modulus and morphology of the crystalline lens: A combined Brillouin optical scanning and OCT study","authors":"Fen Song ,&nbsp;Le Chang ,&nbsp;Shijia Qu ,&nbsp;Shaohu Bai ,&nbsp;Yan Wang","doi":"10.1016/j.exer.2025.110591","DOIUrl":"10.1016/j.exer.2025.110591","url":null,"abstract":"<div><h3>Purpose</h3><div>To explore the correlation between age and in vivo parameters such as the longitudinal modulus of the lens nucleus (LMN), anterior cortex (LMAC), posterior cortex (LMPC), and lens morphology in healthy adults.</div></div><div><h3>Methods</h3><div>A total of 191 right eyes of healthy adults (18–67 years) were included. General demographic information was collected, and Brillouin optical scanning and optical coherence tomography imaging were performed. Correlation and multiple regression analyses were conducted to analyze the factors associated with the lens longitudinal modulus and other parameters. Principal component analysis (PCA) was performed to investigate the relationships between the lens morphological and longitudinal modulus parameters and age.</div></div><div><h3>Results</h3><div>The LMN was positively correlated with age (β = 0.304, P = 0.044), whereas the LMAC and LMPC showed no correlation with age (P &gt; 0.05). The LMN, LMAC, and LMPC were negatively correlated with lens density (LD) (β = −0.794, P &lt; 0.001; β = −0.273, P = 0.033; β = −0.422, P = 0.001). Moreover, the LMN was higher in females than in males (β = 0.159, P = 0.009). PCA revealed that age had greater influence on morphological parameters than on longitudinal modulus parameters (morphological PC1: R² = 0.469 vs. longitudinal modulus PC1: R² = 0.181).</div></div><div><h3>Conclusions</h3><div>Changes in lens morphological parameters in vivo were more closely correlated with age than were its longitudinal modulus parameters. The LMN increased with age, and LD was a key factor influencing the longitudinal modulus.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110591"},"PeriodicalIF":2.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144907965","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":"Comment on “Neuroprotective effects of SIRT1 in human RGCs derived from iPSCs following oxidative stress induction at early and late stages of differentiation”","authors":"Parth Aphale,&nbsp;Himanshu Shekhar,&nbsp;Shashank Dokania","doi":"10.1016/j.exer.2025.110592","DOIUrl":"10.1016/j.exer.2025.110592","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110592"},"PeriodicalIF":2.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886886","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":"Analysis of mouse lens morphological and proteomic abnormalities following deletion of the βB3-crystallin promoter","authors":"Danielle Rayêe ,&nbsp;Phillip A. Wilmarth ,&nbsp;Judy K. VanSlyke ,&nbsp;Keith Zientek ,&nbsp;Ashok P. Reddy ,&nbsp;Linda S. Musil ,&nbsp;Larry L. David ,&nbsp;Aleš Cvekl","doi":"10.1016/j.exer.2025.110587","DOIUrl":"10.1016/j.exer.2025.110587","url":null,"abstract":"<div><div>Crystallin proteins serve as both essential structural and as well as protective components of the ocular lens and are required for the transparency and light refraction properties of the organ. The mouse lens crystallin proteome is represented by αA-, αB-, βA1-, βA2-, βA3-, βA4-, βB1-, βB2-, βB3-, γA-, γB-, γC-, γD-, γE, γF-, γN-, and γS-crystallin proteins encoded by 16 genes. Their mutations are responsible for lens opacification and early onset cataract formation. While many cataract-causing missense and nonsense mutations are known for these genes, including the human <em>CRYBB3</em> gene, the mammalian loss-of function model of <em>Crybb3</em> remains to be established. Herein, we generated the first mouse model via deletion of the <em>Crybb3</em> promoter that nearly abolished expression of the βB3-crystallin. Histological analysis of lens morphology using newborn βB3-crystallin-deficient lenses revealed disrupted lens morphology with early-onset phenotypic variability. In-depth lens proteomics at four time points (newborn, 3-weeks, 6-weeks, and 3-months) showed both down- and up-regulation of various proteins, with the highest divergence from control mice observed in 3-months lenses. Apart from the βB3-crystallin, Smarcc1/Baf155 was down-regulated in all four stages. In addition, downregulation of Hspe1, Pdlim1, Ast/Got, Lsm7, Ddx23, and Acad11 was found in three time points. Finally, we show that the βB3-crystallin promoter region, which contains multiple binding sites for the transcription factors AP-2α, c-Jun, c-Maf, Etv5, and Pax6 is activated by FGF2 in primary lens cell culture experiments. Together, these studies establish the mouse <em>Crybb3</em> loss-of-function model and its disrupted crystallin and non-crystallin proteomes.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110587"},"PeriodicalIF":2.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894775","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":"Corrigendum to “Circ-CARD6 inhibits oxidative stress-induced apoptosis and autophagy in ARPE-19 cells via the miR-29b-3p/PRDX6/PI3K/Akt axis” [(2024) 238 109690 doi: 10.1016/j.exer.2023.109690. Epub 2023 6]","authors":"Xinyu Fan ,&nbsp;Yanni Yang ,&nbsp;Guojiu Wu ,&nbsp;Yanbo Kong ,&nbsp;Yuanping Zhang ,&nbsp;Xu Zha","doi":"10.1016/j.exer.2025.110560","DOIUrl":"10.1016/j.exer.2025.110560","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"259 ","pages":"Article 110560"},"PeriodicalIF":2.7,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882424","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":"Effects of curcumin-liposome formulation on inflammatory cascade activated by oxidative stress in primary human corneal epithelial cells","authors":"Anna M. Roszkowska ,&nbsp;Francesca Polito ,&nbsp;Joanna Wierzbowska ,&nbsp;Laura Licitri ,&nbsp;Irene Gasparo ,&nbsp;Margherita Torre ,&nbsp;Vincenzo Macaione ,&nbsp;Pasquale Aragona ,&nbsp;M'Hammed Aguennouz","doi":"10.1016/j.exer.2025.110584","DOIUrl":"10.1016/j.exer.2025.110584","url":null,"abstract":"<div><div>Curcumin is a naturally occurring polyphenol extracted from turmeric, that exhibits several challenging properties such as anti-inflammatory, antioxidant, lipid-modulating, anti-thrombotic, immunomodulatory, neuroprotective, hepatoprotective and anti-tumor activities. Dry eye disease (DED) is recognized as a multifactorial disorder of the tears and ocular surface, associated with different symptoms, visual disturbance, and tear film instability, accompanied by inflammation of the ocular surface. Inflammation contributes to dry eye disese and in turn dry eyes can lead to worsening inflammation. Protective effects of curcumin have been proved in different eye diseases such as uveitis, idiopathic orbital inflammation, glaucomatous optic neuropathy and diabetes. Considering this background, the aim of the present study was to investigate the effects of curcumin loaded liposomes on human corneal epithelial culture cells subjected to oxidative stress, in order to detect cells’ defensive response to the oxidative stress in presence of curcumin and to determine the optimal concentration of curcumin loaded liposomes for ophthalmic topical therapy in ocular surface disorders. Results obtained demonstrated that curcumin was able to protect cells from oxidative stress induced by hydrogen peroxide by reducing inflammation and activation of TNF-α (p &lt; 0.01 vs H₂O₂ cells), NF-kB (p &lt; 0.01 vs H₂O₂ cells) and NLRP3 (p &lt; 0.01 vs H₂O₂ cells) pathways. Moreover, our results evidenced that curcumin reduced the levels of Bax (p &lt; 0.01 vs H₂O₂ cells), a well known proapoptotic protein, and enhanced Bcl-2 protein (p &lt; 0.01 vs H₂O₂ cells), thus exerting protection against apoptosis in corneal cells. All together, these results confirm the neutralizing effects of curcumin on the oxidative stress induced changes in corneal epithelial cells that might prevent cells damage and death with successive promoting of the inflammatory cascade.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110584"},"PeriodicalIF":2.7,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144872181","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":"Posterior capsular Opacification: Pathogenesis, challenges, and innovative therapeutic strategies","authors":"Yue Wang ,&nbsp;Kai Cao ,&nbsp;Meng Li ,&nbsp;Xiu-Hua Wan","doi":"10.1016/j.exer.2025.110585","DOIUrl":"10.1016/j.exer.2025.110585","url":null,"abstract":"<div><div>Posterior capsular opacification (PCO), a clouding of the lens capsule, can occur as a major complication after cataract surgery. The standard cataract surgical procedure involves the removal of the lens nucleus and cortex, while retaining a portion of the anterior capsule and the complete posterior capsule. Lens epithelial cells (LECs) are difficult to eliminate entirely, and the residual LECs are prone to proliferate and migrate, resulting in light scattering within the visual axis. Despite advancements in surgical interventions and intraocular lens (IOL) designs, PCO remains a widespread issue. The pathophysiological mechanisms underlying PCO primarily involve the proliferation, migration, and epithelial-mesenchymal transition (EMT) of residual LECs, which ultimately culminate in opacification of the posterior capsule. Recent years have witnessed substantial progress in elucidating the pathogenesis of PCO, facilitated by advancements in molecular biology techniques. This review summarizes current research on cellular and molecular mechanisms of PCO, focusing on LEC proliferation, migration, EMT, oxidative stress, extracellular matrix accumulation, and inflammation. Innovative therapeutic strategies, including IOL modifications, pharmacological interventions, and gene therapy, are being explored. Future research endeavors should concentrate on translating foundational research findings into clinical applications to enhance the prognosis for cataract patients.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"259 ","pages":"Article 110585"},"PeriodicalIF":2.7,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144860405","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":"Inhibition of RORγt suppresses both retinal and choroidal neovascularization in mice","authors":"Yujuan Cai ,&nbsp;Siyu Jiang ,&nbsp;Yue Sun ,&nbsp;Nyamjargal Nyambayar ,&nbsp;Ruijie Lin ,&nbsp;Yanji Zhu ,&nbsp;Xiuping Chen ,&nbsp;Bing Xie","doi":"10.1016/j.exer.2025.110573","DOIUrl":"10.1016/j.exer.2025.110573","url":null,"abstract":"<div><div>Retinal and choroidal neovascularization (RNV and CNV) are critical pathological features of vision-threatening ocular disorders. This study investigated the role of retinoic acid receptor-related orphan receptor γt (RORγt) in the regulation of RNV and CNV formation using oxygen-induced retinopathy (OIR) and CNV mouse models, and explored its underlying mechanisms. We demonstrated that RORγt expression was significantly elevated in retinal tissues of both models, co-localizing with IL-23 receptor (IL-23R) and T-cell receptor γδ (TCRγδ), indicating its primary expression in Th17 and γδT cells. Pharmacological inhibition of RORγt with GSK805 effectively reduces pathological NV and leakage, as evidenced by decreased retinal NV areas, vaso-obliteration areas and Evans blue extravasations in the OIR model and reduced vascular leakage and CNV areas in the CNV model. Additionally, GSK805 treatment downregulated pro-inflammatory cytokines (IL-22 and IL-17A), angiogenic factors (angiopoietin 2, PDGF-B, and PDGFR-β), and inflammasome components (NLRP3 and ASC), while modulating macrophage polarization by reducing M1 markers and increasing M2 markers. These findings reveal that RORγt plays a supportive role in NV by influencing key inflammatory and angiogenic pathways, suggesting that RORγt inhibition may represent a promising therapeutic strategy for NV-related retinal diseases.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110573"},"PeriodicalIF":2.7,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144872182","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":"Stachydrine mitigates high glucose-induced apoptosis in human lens epithelial cells by activating mitophagy","authors":"Guijia Wu ,&nbsp;Xiteng Chen ,&nbsp;Wei Wang ,&nbsp;Zhenyu Kou,&nbsp;Han Mao,&nbsp;Yijing Wang,&nbsp;Lijie Dong,&nbsp;Tingting Lin,&nbsp;Fang Tian","doi":"10.1016/j.exer.2025.110568","DOIUrl":"10.1016/j.exer.2025.110568","url":null,"abstract":"<div><div>Diabetic cataract (DC) is a prevalent complication of diabetes. This condition often leads to significant visual impairment and, in some cases, blindness. Recent studies have highlighted the potential protective effects of natural plant extracts in the context of DC. Stachydrine (STA), an alkaloid derived from Leonurus heterophyllus Sweet, has been identified as a natural compound with superior bioavailability and fewer side effects than conventional antioxidants. However, its protective role in high-glucose-induced lens epithelial cell damage remains to be fully elucidated.</div><div>In this study, we established a high-glucose model using HLE-B3 cells and assessed apoptosis following STA treatment. Mitochondrial network morphology was analyzed using the ImageJ software. To further investigate the role of autophagy in STA's effects, we employed the autophagy inhibitor 3-Methyladenine (3-MA). Our results indicated that high glucose exposure decreased autophagosome formation and lysosomal activity, while STA treatment significantly increased both. Furthermore, STA enhanced LC3B expression and reduced P62 levels, counteracting the effects of high glucose. Regarding mitochondrial morphology, STA effectively restored the shape, branching, and area, all of which were diminished by high glucose exposure.</div><div>Additionally, STA effectively ameliorated mitochondrial network damage induced by high glucose. Notably, when the cells were treated with 3-MA, STA's protective effects on apoptosis and mitochondrial morphology were significantly reversed. In conclusion, our findings suggest that STA exerts protective effects against high-glucose-induced damage by regulating mitophagy, and this autophagy-dependent mechanism may hold therapeutic potential for the treatment of diabetic cataract.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110568"},"PeriodicalIF":2.7,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859067","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":"Targeting LARP1 to mitigate aging in lens epithelial cells: mechanistic insights into mitochondrial dysfunction","authors":"Hang Qi ,&nbsp;Liankun Sun ,&nbsp;Jiannan Chai ,&nbsp;Jiaoyan Ma ,&nbsp;Huimei Yu ,&nbsp;Meihui Xia ,&nbsp;Xiaoqing Hu","doi":"10.1016/j.exer.2025.110582","DOIUrl":"10.1016/j.exer.2025.110582","url":null,"abstract":"<div><div>As we age, lens epithelial cells (LECs) undergo various stressors, contributing to cataract development. Targeting the regulation of mitochondrial metabolism may be an effective strategy to delay LEC aging. La-related protein 1 (LARP1) is an RNA-binding protein that affects mitochondrial function by regulating mRNA stability and translation. However, the specific mechanism underlying the role of LARP1 in LEC aging is unclear. In the present study, we found that LARP1 was significantly upregulated during D-galactose-induced senescence in LECs. LARP1 knockdown significantly attenuated cellular senescence and restored mitochondrial oxidative phosphorylation (OXPHOS) function. Further studies revealed that the upregulation of LARP1 inhibited the expression of the nuclear-encoded OXPHOS subunits NDUFB8 and SDHB, thereby impairing OXPHOS function. LARP1 inhibited translation of NDUFB8 and SDHB mRNAs by binding to these mRNAs and forming stress granules (SGs). In the presence of SG inhibitors, the translation levels of NDUFB8 and SDHB were restored, and cellular senescence markers were significantly reduced. In conclusion, the present study revealed the critical role of LARP1 in LEC senescence, suggesting that it impairs mitochondrial OXPHOS function through SG-mediated translational inhibition, which provides new insights into the mechanism of mitochondrial dysfunction in LEC senescence, as well as new intervention strategies to resist LEC senescence.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110582"},"PeriodicalIF":2.7,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862232","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":"MTHFD2 drives retinoblastoma progression via Notch signaling activation: Implications for targeted pediatric ocular cancer therapy","authors":"Chunyue Yao ,&nbsp;Tingting Chen ,&nbsp;Yijia Chen ,&nbsp;Weiqi Wu ,&nbsp;Yingjie Li ,&nbsp;Yanyan Zhang ,&nbsp;Guofu Huang","doi":"10.1016/j.exer.2025.110579","DOIUrl":"10.1016/j.exer.2025.110579","url":null,"abstract":"<div><div>Retinoblastoma (RB), the most prevalent intraocular malignancy in children, severely threatens vision and survival, yet therapeutic strategies for recurrent or refractory RB remain limited. MTHFD2 (Methylenetetrahydrofolate Dehydrogenase 2), one of the key enzymes involved in mitochondrial one-carbon metabolism, is aberrantly overexpressed in multiple cancers. Elevated MTHFD2 expression correlates with poor prognosis in various malignancies, and its depletion significantly suppresses tumor invasiveness and induces programmed cell death. However, whether MTHFD2 contributes to RB progression remains largely unexplored. Here, we reported that MTHFD2 expression was markedly upregulated in RB tissues and cell lines (Y79, Weri-RB1). <em>In vitro</em> functional assays demonstrated that MTHFD2 overexpression suppressed apoptosis and enhanced RB cell viability, colony formation, whereas MTHFD2 knockdown promoted apoptosis and inhibited RB cell viability, colony formation. In terms of mechanism, RNA sequencing and KEGG analysis revealed that differentially expressed genes (DEGs) were significantly enriched in pathways related to tumorigenesis. Meanwhile, we further demonstrated that MTHFD2 drove tumor progression by activating the Notch signaling pathway. Additionally, <em>In vivo</em> studies confirmed that MTHFD2 downregulation suppressed tumor graft growth and reduced expression of tumor proliferation marker Ki67. Our findings validate the critical oncogenic properties of MTHFD2 in RB by sustaining cell proliferation and preventing apoptosis. The tumor-promoting effects of MTHFD2 are likely mediated via the Notch signaling cascade, highlighting its potential as a therapeutic target for RB treatment.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"260 ","pages":"Article 110579"},"PeriodicalIF":2.7,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859066","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}