Experimental eye research最新文献

{"title":"Deep learning-based diagnostic classification of multiple sclerosis using multicenter optical coherence tomography data","authors":"Zahra Khodabandeh ,&nbsp;Hossein Rabbani ,&nbsp;Neda Shirani Bidabadi ,&nbsp;Fereshteh Ashtari ,&nbsp;David H. Steel ,&nbsp;Jaume Bacardit ,&nbsp;Anya Hurlbert ,&nbsp;Raheleh Kafieh","doi":"10.1016/j.exer.2026.110916","DOIUrl":"10.1016/j.exer.2026.110916","url":null,"abstract":"<div><h3>Background</h3><div>Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system, where timely and accurate diagnosis is essential for effective management. Optical coherence tomography (OCT) enables non-invasive evaluation of retinal changes that may serve as biomarkers for MS. Unlike other ophthalmologic diseases, raw cross-sectional OCT images in MS show subtle alterations often indistinguishable from healthy controls (HCs). Consequently, retinal layer thickness and boundary-derived surface features offer greater discriminatory power.</div></div><div><h3>Methods</h3><div>We investigated three categories of artificial intelligence (AI) models: (1) feature extraction with auto-encoder (AE) and shallow networks, (2) custom-designed deep networks, and (3) fine-tuned pre-trained networks. Retinal layer thickness and surface maps derived from OCT were analyzed to determine the most informative features, with channel-wise combination and mosaicing applied for feature integration. Model interpretability was assessed using occlusion sensitivity and Gradient-weighted Class Activation Mapping (Grad-CAM) visualizations. The dataset included 38 HC and 78 MS eyes obtained from independent public and local sources. Patient-wise partitioning was implemented to prevent data leakage.</div></div><div><h3>Results</h3><div>The proposed deep network using channel-wise combined thickness maps of retinal nerve fiber layer (RNFL), ganglion cell and inner plexiform layer (GCIPL), and inner nuclear layer (INL) layers achieved balanced accuracy of 97.3% (SD = 4.16; 95% CI: 92.3–100%), specificity of 97.3% (SD = 5.59; 95% CI: 92.6–100%), sensitivity of 97.4% (SD = 3.54; 95% CI: 92.6–100%), g-mean of 97.3% (SD = 4.18; 95% CI: 92.24-100%), F1-score of 98.0% (SD = 3.86; 95% CI: 92.6–100%), and an AUC of 0.96 (SD = 0.08; 95% CI: 0.95–1.00). Notably, the high performance observed in internal cross-validation was achieved when public and local datasets were combined. However, performance decreased substantially in cross-dataset evaluations, where models were trained on one dataset and tested on the other, indicating limited external generalizability, particularly when trained on public data and applied to local clinical data.</div></div><div><h3>Conclusions</h3><div>AI-based analysis of OCT-derived retinal layer features enables accurate and interpretable classification of MS, supporting its potential as a valuable clinical biomarker.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110916"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178443","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 comments on “Circadian rhythm disruption induces myopia in mice”","authors":"Wei-Ling Bai ,&nbsp;Mei-Jun Wang ,&nbsp;Jia-He Gan ,&nbsp;Ying Huang ,&nbsp;Zi-Han Liu ,&nbsp;Cong-Ying Li ,&nbsp;Ning-Li Wang ,&nbsp;Shi-Ming Li","doi":"10.1016/j.exer.2026.110889","DOIUrl":"10.1016/j.exer.2026.110889","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110889"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156478","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":"Role of NDUFS1 in mitochondrial dysfunction and oxidative stress in glaucomatous retinal ganglion cells","authors":"Jing Zhang ,&nbsp;Lin Jiang ,&nbsp;Xiao Zheng","doi":"10.1016/j.exer.2026.110913","DOIUrl":"10.1016/j.exer.2026.110913","url":null,"abstract":"<div><div>This study investigates the role of NDUFS1, a subunit of mitochondrial complex I, in glaucomatous retinal ganglion cell (RGC) injury and determines whether it mediates RGC apoptosis through regulating mitochondrial dysfunction and oxidative stress (OS). A microbead-induced glaucoma mouse model was established. Intraocular pressure (IOP) measurements, retinal whole-mount immunofluorescence staining, TUNEL assay, and OS marker detection were conducted to assess RGC survival, apoptosis, and OS. <em>In vitro</em>, NDUFS1 was knocked down or overexpressed in R28 retinal cells. JC-1 staining, adenosine triphosphate (ATP) assay, and flow cytometry were employed to analyze the impacts of NDUFS1 on mitochondrial membrane potential, energy metabolism, OS, and apoptosis. Finally, adeno-associated virus-mediated NDUFS1 overexpression (AAV-oe-NDUFS1) was delivered via intravitreal injection to validate its protective effects <em>in vivo</em>. <em>In vivo</em> experiments revealed downregulation of NDUFS1 expression in the retinas of glaucoma mice, accompanied by significant RGC loss, enhanced OS, and increased apoptosis. <em>In vitro</em>, NDUFS1 knockdown induced mitochondrial membrane depolarization, reduced ATP synthesis, exacerbated OS, and ultimately promoted apoptosis. Conversely, NDUFS1 overexpression effectively reversed these pathological phenotypes. Rescue experiments <em>in vivo</em> further demonstrated that NDUFS1 upregulation alleviated OS, suppressed apoptosis, and significantly improved RGC survival. NDUFS1 downregulation plays a critical role in glaucomatous RGC injury. Overexpression of NDUFS1 improves mitochondrial function, attenuates OS, and enhances cell survival. The study provides novel mechanistic insights into neuroprotection in glaucoma and suggests NDUFS1 as a potential therapeutic target.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110913"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164736","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":"Effect of chemokine and chemokine-receptor gene polymorphisms on the development of diabetic retinopathy in the Turkish cohort","authors":"Ebru Alp ,&nbsp;Egemen Akgun ,&nbsp;Sibel Doguizi ,&nbsp;Fadime Mutlu Icduygu ,&nbsp;Mehmet Ali Sekeroglu ,&nbsp;Murat Atabey Ozer","doi":"10.1016/j.exer.2026.110912","DOIUrl":"10.1016/j.exer.2026.110912","url":null,"abstract":"<div><div>It is known that in many acute and chronic inflammatory diseases, chemokines are secreted into the environment and increase during the inflammation process. Inflammation is thought to be important in the pathogenesis of diabetic retinopathy (DR) and various cytokines and chemokines play a role. Accordingly, the aim of the present study is to determine the relationship between DR and chemokines and their receptor gene polymorphisms (CXCL12, CXCR4, CCL2, CCR2) in Turkish population. This study included 353 patients with type 2 diabetes mellitus (with and without retinopathy) and 204 controls. Genomic DNA was isolated from whole blood and genotype distribution of polymorphisms was determined by PCR-RFLP method. It was determined that the G allele of the CCL2 rs1024611 SNP could prevent the development of DR (1.42 fold) and PDR (proliferative diabetic retinopathy) (1.92 fold). Binary logistic regression analysis also showed that the TT genotype of CXCL12 rs1801157 SNP may have a protective effect (OR = 0.258) on the development of DR. In contrast, CXCR4/rs2228014 and CCR2/rs1799864 SNPs did not show a significant effect on DR in the Turkish population. Findings of the present study suggest that the CCL2 rs1024611 SNP may play a role in the etiology of DR and PDR, and the G allele has a protective effect in Turkish population. Furthermore, TT genotype of CXCL12 rs1801157 SNP may also provide protection against the development of DR. Large-scale studies including a large number of patients are recommended to confirm these results.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110912"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156484","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":"Re-evaluating “Circadian rhythm disruption induces myopia in mice”: The need to consider sex as a biological variable in translational myopia research","authors":"Gang Chen,&nbsp;Yixia Zhang","doi":"10.1016/j.exer.2026.110888","DOIUrl":"10.1016/j.exer.2026.110888","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110888"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100179","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":"Fundus albipunctatus disease-associated RDH5/L310delinsEV mutation undertakes AMFR-mediated polyubiquitination and degradation in proteasome","authors":"Yichen Dong ,&nbsp;Rong Xue ,&nbsp;Yi Zhang ,&nbsp;Xiaolin Jia ,&nbsp;Mingjun Jiang ,&nbsp;Mengjiao Xue ,&nbsp;Xuyan Peng ,&nbsp;Guangming Wan ,&nbsp;Yanzhong Hu","doi":"10.1016/j.exer.2026.110927","DOIUrl":"10.1016/j.exer.2026.110927","url":null,"abstract":"<div><div>Genetic mutations in <em>retinol dehydrogenase 5</em> (<em>RDH5</em>) are associated with the inherited autosomal recessive retinal degeneration diseases, especially fundus albipunctatus (FA). Most of RDH5 mutants exhibit downregulation of RDH5 protein expression. However, the regulatory mechanism remains unclear. Here, we studied the metabolism of RDH5/L310delinsEV mutation, an indel mutation closely associated with the inherited FA disease. The half-life of RDH5/L310delinsEV was much less than RDH5/WT. Unlike RDH5/WT, which normally underwent degradation in autophagy-lysosomes, the RDH5/L310delinsEV reduced its location to the endoplasmic reticulum and was easy to be polyubiquitinated and degraded in the ubiquitin-proteasome pathway. Both RDH5/WT and RDH5/L310delinsEV interacted with autocrine motility factor receptor (AMFR), which is an E3 ligase on the endoplasmic reticulum. Overexpression of or knockdown of AMFR by siRNA increased or reduced the degradation of RDH5/L310delinsEV. The lysine 179 and lysine 263 of RDH5/L310delinsEV protein were polyubiquitination sites by AMFR. Mutation of K179R and K263R in RDH5/L310delinsEV protein reduced AMFR-mediated polyubiquitination and degradation. Taken together, these results highlight that RDH5/L310delinsEV mutant in RDH5 causes a rapid degradation in the ubiquitin-proteasome pathway. The fast degradation of RDH5/L310delinsEV may be associated with the FA development.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110927"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178452","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 hypoxia-mediated HIF-1α/miR-381-3p signaling pathway promotes retinal neovascularization","authors":"Qingguo Guo ,&nbsp;Xin Xu ,&nbsp;Qicheng Tian ,&nbsp;Haoran Zhu ,&nbsp;Lei Pei ,&nbsp;Guangzuo Luo ,&nbsp;Ying Liu","doi":"10.1016/j.exer.2026.110925","DOIUrl":"10.1016/j.exer.2026.110925","url":null,"abstract":"<div><div>Retinal neovascularization is a common pathological feature of various retinal vascular diseases and is typically induced by hypoxia. In recent studies, the regulatory role of microRNA (miRNA)-mediated signaling in retinal neovascularization has been extensively characterized. However, although hypoxia-induced miRNA dysregulation has been identified, the specific mechanisms by which hypoxia modulates miRNAs in retinal neovascularization remain largely elusive. In this study, we first established a direct regulatory link between microRNA-381-3p (miR-381-3p) and hypoxia-inducible factor-1α (HIF-1α) using a dual-luciferase reporter gene assay. Based on an <em>in vitro</em> cellular hypoxia model and an <em>in vivo</em> oxygen-induced retinopathy (OIR) mouse model, we validated the regulatory effect of HIF-1α on miR-381-3p expression. In addition, downregulation of miR-381-3p attenuated retinal neovascularization, inflammation, and apoptosis in OIR mice. Transcriptome sequencing analysis identified Steap4, a differentially expressed gene, as a potential downstream target of miR-381-3p. Further detection suggested that inhibition of miR-381-3p expression could down-regulate the expression of STEAP4 both <em>in vitro</em> and in <em>vivo</em>. Collectively, our study provides compelling evidence that the HIF-1α/miR-381-3p pathway plays a critical regulatory role in retinal neovascularization, which complements the pathogenic mechanisms underlying retinal vascular diseases and suggests that miR-381-3p may serve as a potential therapeutic target for treating retinal neovascularization.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110925"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178510","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":"PIKfyve is an essential component of the endolysosomal pathway within photoreceptors and the retinal pigment epithelium","authors":"Karen Attia ,&nbsp;Ifrah Anjum ,&nbsp;Susanne Lingrell ,&nbsp;Chavy Dworkind ,&nbsp;Matthew D. Benson ,&nbsp;Ian M. MacDonald ,&nbsp;Jennifer C. Hocking","doi":"10.1016/j.exer.2026.110905","DOIUrl":"10.1016/j.exer.2026.110905","url":null,"abstract":"<div><div>Phosphoinositides (PIs) are a family of seven low abundance membrane lipids, each with distinct signaling functions. The phosphoinositide kinase PIKfyve generates phosphoinositide-3,5-bisphosphate (PI(3,5)P₂) and PI5P. Emerging evidence implicates PIKfyve in key cellular processes, including autophagy, phagocytosis, endosomal trafficking, lysosomal maintenance, and melanosome formation. Complete loss of PIKfyve function is embryonic lethal in model organisms. In humans, heterozygous mutations in <em>PIKFYVE</em> are associated with Fleck corneal dystrophy and congenital cataracts. In this study, we investigate the role of PIKfyve in photoreceptors and the adjacent retinal pigment epithelium (RPE), host to dynamic endolysosomal pathways required for enduring the high oxidative stress environment, transporting metabolites and phototransduction components, and the breakdown of outer segment discs. To assess PIKfyve function in the retina and RPE in our zebrafish model, we employed CRISPR/Cas9-mediated gene editing and pharmacological inhibition using the specific PIKfyve inhibitor apilimod. Loss of PIKfyve activity leads to RPE expansion characterized by the accumulation of LC3- and LAMP1-positive vacuoles, along with defects in phagosome degradation and minor changes to melanosome biogenesis. Photoreceptors deprived of PIKfyve function develop a single large vacuole in the inner segment, while the OS remains largely intact over the timespan analyzed. Electroretinography (ERG) recordings revealed complete visual impairment in <em>pikfyve</em> crispant larvae and significantly reduced visual function in larvae treated with apilimod post embryogenesis. These findings highlight the critical role of PIKfyve in the development and homeostasis of the RPE and retina.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110905"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124355","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":"Modified Autologous Conditioned Serum (mACS) demonstrates the neuroprotective effect in the Benzalkonium chloride (BAK)-induced murine dry eye model","authors":"En-Chia Mai ,&nbsp;Kuo-Hsuan Hung ,&nbsp;Shao-Hsuan Chang ,&nbsp;Chun Hsiung ,&nbsp;Chung-Chuan Hsiung ,&nbsp;Lung-Kun Yeh","doi":"10.1016/j.exer.2026.110898","DOIUrl":"10.1016/j.exer.2026.110898","url":null,"abstract":"<div><div>The purpose of this study was to analyze and compare cytokine and growth factor levels in modified autologous conditioned serum (mACS) and autologous serum (AS) and to evaluate their therapeutic effects in a benzalkonium chloride (BAK)-induced murine dry eye model. Serum samples were obtained from twenty healthy volunteers and analyzed by ELISA. A dry eye model was established in twenty-four C57BL/6 mice by topical application of 0.2% BAK twice daily for seven days. The mice were evenly divided into three subgroups: saline-treated, 0.5% AS-treated, and 0.5% mACS-treated. The right eyes were treated, and the left eyes served as untreated controls. Eyeballs were harvested on days 7 and 14 for immunofluorescence staining. Results showed that neuroprotective factors (BDNF and fractalkine), pro-inflammatory cytokines (IL-1β, IL-6, MIF, TNF-α), and VEGF-A were significantly elevated in the mACS group, whereas PDGF-BB was significantly reduced. Furthermore, immunofluorescence analysis demonstrated a significantly greater recovery of central corneal nerve fibers in the mACS-treated group compared with the saline group at day 7 (p &lt; 0.01).</div><div>At day 14, the mACS-treated group continued to show a trend toward increased central corneal nerve regeneration, although this difference did not reach conventional statistical significance (p &lt; 0.1). No significant differences were observed between the AS- and saline-treated groups. In conclusion, compared with AS, mACS demonstrates a cytokine profile suggestive of enhanced neuroprotective potential and may facilitate corneal nerve regeneration in the BAK-induced murine dry eye model.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110898"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131627","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":"Decreased corneal biomechanical stability and structural integrity in PPAR-α knockout mice","authors":"Chengfang Zhu ,&nbsp;Huan He ,&nbsp;Hongwei Yan ,&nbsp;Aolin Liu ,&nbsp;Minghui Liang ,&nbsp;Rongrong Zong ,&nbsp;Bin Liu ,&nbsp;Xiuxian Qin ,&nbsp;Juan Yang ,&nbsp;Zhirong Lin","doi":"10.1016/j.exer.2026.110911","DOIUrl":"10.1016/j.exer.2026.110911","url":null,"abstract":"<div><div>Recent evidence indicates that inflammatory cytokines and proteolytic enzymes play a vital role in the development of biomechanical failure in the cornea. Previous studies have shown that inflammatory cascades could be inhibited by peroxisome proliferator-activated receptor-α activation. This study seeks to investigate the biomechanical and structural features of the cornea in PPAR-α−/− mice and to assess alterations in inflammatory cytokines and enzymes. Adult PPAR-α^−/− mice and wild-type C57BL/6 mice (WT) were used in this study. The corneas were excised and evaluated by modulus of elasticity test, enzymatic tissue digestion assay, corneal fluorescein sodium staining, tear film break-up time (tBUT), anterior segment OCT, in vivo corneal confocal microscopy (IVCM), transmission electron microscopy (TEM), and quantitative real-time PCR (RT-PCR). Decreased tBUT and SIt values were observed, while no corneal lesions were observed in the PPAR-α^−/− mice. The corneal tangent modulus at fracture and resistance to enzymatic hydrolysis in PPAR-α^−/− mice were significantly decreased (<em>P</em> = 0.005 and <em>P</em> &lt; 0.001, respectively). Anterior segment OCT showed that the corneas of PPAR-α^−/− mice were significantly thinner than in the WT (<em>P</em> = 0.008). IVCM showed that the corneal nerve fibers of PPAR-α^−/− mice were slender, and the hypo-reflective folds of the stromal layer were more apparent, while the stromal fibers of the WT were thicker. TEM showed that the lamellar stromal fibers were interlaced and disorganized with decreased fiber density in PPAR-α^−/− mice compared with the WT. The expression of F-actin, lumican, laminin, TGF-β, TIMP-1, and TIMP-3 in the cornea of PPAR-α^−/− mice was also decreased, accompanied by an increase of TNF-α and MMP-9. In conclusion, the corneal biomechanical stability and microstructural integrity of PPAR-α^−/− mice were decreased, which might be associated with dysregulation of corneal structure-related components, inflammation-related factors, and proteases.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110911"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164709","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}