Experimental eye research最新文献

{"title":"Involvement of TGF-β signaling pathway-associated genes in the corneal endothelium of patients with Fuchs endothelial corneal dystrophy","authors":"Tatsuya Nakagawa ,&nbsp;Tetsuro Honda ,&nbsp;Soichiro Inagaki ,&nbsp;Taichi Yuasa ,&nbsp;Theofilos Tourtas ,&nbsp;Ursula Schlötzer-Schrehardt ,&nbsp;Friedrich Kruse ,&nbsp;Ines Aouimeur ,&nbsp;Hanielle Vaitinadapoule ,&nbsp;Gauthier Travers ,&nbsp;Zhiguo He ,&nbsp;Philippe Gain ,&nbsp;Noriko Koizumi ,&nbsp;Gilles Thuret ,&nbsp;Naoki Okumura","doi":"10.1016/j.exer.2025.110334","DOIUrl":"10.1016/j.exer.2025.110334","url":null,"abstract":"<div><div>This study investigated the involvement of TGF-β signaling pathway-associated genes in the pathogenesis of Fuchs endothelial corneal dystrophy (FECD). The RNA-sequencing analysis of corneal endothelial cells (CECs) from FECD patients revealed significant alterations in multiple TGF-β superfamily genes, with 9 genes upregulated (including BMP6, GDF5, and TGF-β2) and 10 genes downregulated (including BMP2, NOG, and INHBA) compared to controls. Quantitative PCR validation confirmed the elevated expression of GDF5 (3.35-fold in non-expanded and 7.66-fold in expanded TCF4), TGF-β2 (6.17-fold and 11.5-fold), and TGF-β1 (1.78-fold and 1.58-fold) in FECD patients with and without TCF4 trinucleotide repeat expansion. Ex-vivo experiments using donor corneas demonstrated that TGF-β2 stimulation significantly increased the expression of extracellular matrix (ECM) components associated with guttae formation, including fibronectin, types I and VI collagens, and other matrix proteins. Immunofluorescence confirmed increased fibronectin protein expression in the corneal endothelium following TGF-β1 or TGF-β2 treatment. This study provides the first comprehensive analysis of TGF-β superfamily involvement in FECD and suggests that GDF5, found to be upregulated in FECD, may contribute to the disease process. These findings further indicate that dysregulation of TGF-β signaling pathways drives the characteristic ECM accumulation in FECD, potentially offering new therapeutic targets for this progressive corneal disease involving fibrosis-related alterations. Future research is warranted to clarify GDF5's specific role and mechanistic impact on FECD pathogenesis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"255 ","pages":"Article 110334"},"PeriodicalIF":3.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624002","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":"Dynamic in vivo mapping of the gradient refractive index and strain distribution of the human lens under accommodative stress","authors":"Sabine Kling ,&nbsp;Vahoura Tahsini ,&nbsp;Farhad Hafezi","doi":"10.1016/j.exer.2025.110332","DOIUrl":"10.1016/j.exer.2025.110332","url":null,"abstract":"<div><div>The mechanical properties and refractive index (RI) distribution within the human crystalline lens are essential for understanding accommodation and age-related changes in the lens. However, there is limited knowledge about how these properties change in vivo with accommodative demand and aging. Previous methods lacked the ability to simultaneously measure both RI and mechanical strain in the lens, limiting their ability to capture the full complexity of the lens' behavior. To address this gap, we measured the spatial distribution of the RI and mechanical strain in the lenses of six healthy participants (aged 24–45 years) using optical coherence tomography (OCT) under three accommodative demands (0, −2, and −4 diopters). A phase-based signal processing algorithm was developed to compute the RI at each pixel of the OCT B-scans, while instantaneous and accumulated strains were used to assess the lens's mechanical properties during micro-fluctuations.</div><div>Our results indicated an axial RI gradient, with the highest RI values in the posterior half of the lens. The RI did not significantly change with age or accommodative demand in participants under 45. However, the instantaneous strain, representing the deformation speed, decreased with age, while the accumulated strain during micro-fluctuations increased with higher accommodative demands. No correlation was observed between the RI and mechanical strain distribution within the lens.</div><div>These findings suggest that OCT is a promising high-resolution tool for in vivo optomechanical characterization of the crystalline lens, offering valuable patient-specific data. OCT could be instrumental in future studies of lenticular changes during emmetropization and myopization.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"255 ","pages":"Article 110332"},"PeriodicalIF":3.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624101","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":"Monitoring mutant myocilin secretion and localization in trabecular meshwork cell cultures using a protein complementation-based luminescence assay","authors":"Hannah A. Youngblood ,&nbsp;Ethan F. Harris ,&nbsp;Kaylee P. Lankford ,&nbsp;Victoria Garfinkel ,&nbsp;John D. Hulleman ,&nbsp;Raquel L. Lieberman","doi":"10.1016/j.exer.2025.110333","DOIUrl":"10.1016/j.exer.2025.110333","url":null,"abstract":"<div><div>Approximately 2–4 % of adult onset and 10 % of juvenile onset cases of primary open angle glaucoma can be attributed to non-synonymous coding mutations in <em>MYOC</em>. One of the key characteristics of a pathogenic <em>MYOC</em> mutant is the inability of the resulting protein to be secreted from trabecular meshwork cells. Instead, pathogenic myocilin variants accumulate in the endoplasmic reticulum. Typically, localization of MYOC mutants is compared to wild-type myocilin in cellular secretion assays that use immunoblot to detect myocilin in extracellular media, alongside intracellular soluble and insoluble (aggregated) fractions. Here, we implement a new method that utilizes a complement-based luminescence method in which an 11-residue HiBiT tag is appended to myocilin and complements a truncated nanoluciferase. The method allows for highly sensitive luminescence detection and does not require immunoblot. We tested non-synonymous coding variants T377R, D384G, D395ins, C433Y, T455K, and L486F, in an established immortalized trabecular meshwork cell line. Secretion was tested in 96-well plate format, revealing poor secretion for these mutants compared to wild-type myocilin. For assays conducted in 6-well plates, myocilin mutants were accumulated in intracellular fractions. HiBiT luminescence signals correlated well with immunofluorescence as well as immunoblot but is more sensitive than the latter. Overall, our study demonstrates that complement-based detection of mutant myocilin using luminescence allows for facile and sensitive detection of myocilin localization and has confirmed secretion defects for six variants.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"255 ","pages":"Article 110333"},"PeriodicalIF":3.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624003","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":"Biomechanical contributions to murine lens shape: Confinement, compaction, and residual stresses","authors":"Matthew A. Reilly","doi":"10.1016/j.exer.2025.110331","DOIUrl":"10.1016/j.exer.2025.110331","url":null,"abstract":"<div><div>Presbyopia is the progressive loss of near vision with age and affects nearly everyone by age 50. This most common visual deficit is a result of age-related changes in lens shape and refractive index, which dictate the optical power of the fully accommodated lens. Lens shape in the absence of external loads is dictated by the balance of biomechanical forces between the lens and its capsule. These residual stresses arise from differential growth. However, these stresses remain unknown. This study uses the nearly spherical murine lens as a model for elucidating how these residual stresses may be calculated and which experimental parameters must be measured to enable such calculations. Several key concepts arise from the analysis in agreement with recent studies. It is suggested that the lens fiber cells are poroelastic and that fiber cell compaction arises from biomechanical confinement effects of the lens capsule. It is possible to computationally “recapsulate” the uncompacted lens after growth, then estimate the extent to which the capsule compacts the fiber cells and, in turn, the extent to which the fiber cells distend the capsule. The simple biomechanical models presented are capable of predicting residual stresses in line with published experimental measurements, suggesting that they capture the essence of how the lens and capsule push and pull during years of differential growth.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"255 ","pages":"Article 110331"},"PeriodicalIF":3.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in keratoconus animal models: From genetics to biomechanics","authors":"Zongzheng Zou ,&nbsp;Shanshan Li ,&nbsp;Haixia Zhang","doi":"10.1016/j.exer.2025.110330","DOIUrl":"10.1016/j.exer.2025.110330","url":null,"abstract":"<div><div>Keratoconus is a disorder characterized by thinning and protrusion of the cornea into a cone shape, potentially leading to decreased vision and blindness. Understanding the pathogenesis of keratoconus and developing treatment strategies is crucial. Currently, animal models of keratoconus created through gene knockout and collagenase digestion have made significant progress in studying the pathogenesis of the disease. However, these models have limitations, such as unverified long-term effects. Future research should focus on optimizing the construction methods of animal models and enhancing long-term observation and evaluation to more accurately simulate human keratoconus. This paper reviews research progress on animal models of keratoconus, examining models constructed using methods such as gene editing, drug induction, cutting of corneal stroma, and mechanical stimulation.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"254 ","pages":"Article 110330"},"PeriodicalIF":3.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624099","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":"Experimental validation of the molecular mechanism of phlorizin in the treatment of diabetic retinopathy","authors":"Lulu Xie ,&nbsp;Ru Zhang ,&nbsp;Chunjie Hu ,&nbsp;Ting Li ,&nbsp;Zhao-Peng Zhang ,&nbsp;Mei-Ying Jin ,&nbsp;Rui Gao ,&nbsp;Zhi-Run Zhang ,&nbsp;Wei Zheng ,&nbsp;Yuan Ju ,&nbsp;Jun-Peng Guo","doi":"10.1016/j.exer.2025.110329","DOIUrl":"10.1016/j.exer.2025.110329","url":null,"abstract":"<div><div>This study conducted an experiment to scrutinize the effect of phlorizin (Phl) on diabetic retinopathy (DR) and to delve into the related molecular mechanisms. Within this investigation, DR was induced in rats with diabetes mellitus (DM) by subjecting them to a regimen involving a high-fat and high-sugar diet, coupled with intraperitoneal administration of streptozotocin (STZ) at a dosage of 45 mg/kg. Retinal damage in DR rats was assessed by means of hematoxylin and eosin (HE) staining. The serum levels of inflammatory and angiogenic factors were also measured. Additionally, the levels of tight junction proteins, angiogenic proteins, and inflammatory proteins in the retinas of DR model rats were assessed using Western blot (WB),immunohistochemistry(IHC) and immunofluorescence(IF). Moreover, bioinformatics and network pharmacology methodologies were utilized to pinpoint intersecting genes linked to DR and to elucidate the mechanism of action of Phl. This involved screening with Venny, conducting Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG)analyses, constructing a Protein-Protein Interaction (PPI) network, and performing molecular docking analysis. The results of this study demonstrated that Phl significantly normalized fasting glucose levels and reduced body weight, thereby alleviating obesity in DR rats after 12 weeks. Furthermore, the serum levels of inflammatory and angiogenic factors were considerably reduced in the drug-treated rats. WB, IHC and IF revealed increased expression of the tight junction proteins zonula occludens-1(ZO-1) and occludin in the retinas of drug-treated DR rats, validating the observed findings. Molecular biology validation experiments based on the predictions by network pharmacology indicated a substantial decrease in the expression levels of vascular endothelial growth factor (VEGF), notch homolog 1 (Notch1), and hypoxia inducible factor-1 (HIF-1α) in the retina upon treatment with Phl. This reduction resulted in the inhibition of neovascularization. Furthermore, Phl exhibited inhibitory effects on inflammatory pathways, leading to a decrease in cytokine release. The overexpression of VEGF was identified as a factor diminishing brain-derived neurotrophic factor(BDNF) expression while increasing the expression levels of inflammatory proteins. Therefore, the results of this research demonstrate that Phl has the potential to protect the retina of DR rats by inhibiting VEGF expression. This protective effect may be associated with the modulation of the VEGF/BDNF/NF-κB signaling pathway.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"254 ","pages":"Article 110329"},"PeriodicalIF":3.0,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585112","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":"SIRT3 mitigates dry eye disease through the activation of autophagy by deacetylation of FOXO1","authors":"Di Zhang ,&nbsp;Qi Liang ,&nbsp;Jiaxuan Jiang ,&nbsp;Wei Liu ,&nbsp;Yiran Chu ,&nbsp;Zeying Chen ,&nbsp;Boda Li ,&nbsp;Taige Chen ,&nbsp;Jia-Ruei Tsao ,&nbsp;Kai Hu","doi":"10.1016/j.exer.2025.110328","DOIUrl":"10.1016/j.exer.2025.110328","url":null,"abstract":"<div><div>Dry eye disease (DED) is a complex ocular condition characterized by oxidative stress, inflammation, and apoptosis. An increasing number of studies suggest that Sirtuin3 (SIRT3), a mitochondrial deacetylase, may offer protection against related pathologies. Despite these indications, the precise function and underlying mechanisms of SIRT3 in the context of DED have not been fully elucidated. Here, we observed a decline in SIRT3 expression in human corneal epithelial cells (HCE-Ts) and the corneal conjunctiva of mice as the disease advanced. Overexpression of SIRT3 in HCE-Ts reduced the accumulation of reactive oxygen species (ROS), inflammatory cytokines, and the rate of apoptosis, while its inhibition had the opposite effect. Importantly, the function of SIRT3 was exerted through the enhancement of autophagic flux. Further studies have shown that chloroquine-induced inhibition of autophagy neutralized the beneficial effects of SIRT3. In our <em>in vivo</em> experiments, the application of eye drops containing a SIRT3 agonist ameliorated the symptoms of DED and increased corneal autophagy in mice. Mechanistically, our study identified that the deacetylation and nuclear translocation of FOXO1 (Forkhead box O1) are pivotal for the SIRT3-mediated enhancement of autophagic flux. These findings posit that SIRT3 as an encouraging therapeutic target for DED, offering new insights into the disease's underlying mechanisms.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"254 ","pages":"Article 110328"},"PeriodicalIF":3.0,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596520","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":"Color vision-associated environmental and biological factors in the development of myopia","authors":"Dongjie Song ,&nbsp;Qianjie Yang ,&nbsp;Jiayun Ge ,&nbsp;Kuangqi Chen ,&nbsp;Jianping Tong ,&nbsp;Ye Shen","doi":"10.1016/j.exer.2025.110324","DOIUrl":"10.1016/j.exer.2025.110324","url":null,"abstract":"<div><div>As a global public health problem, myopia has attracted more and more attention for its high prevalence and severe visual impairment. Although extensive research on the risk factors for myopia has been conducted, the underlying pathogenesis is still unclear. Color vision, mediated by retinal cone cells, is a fundamental and important component of human visual functions. Indeed, numerous studies implicate color vision-associated environmental and biological factors in myopia pathogenesis, indicating that related interventions may delay myopia progression. Studies have shown that color vision can induce different accommodation responses under near work conditions and exert opposite effects in different light environments to influence myopia advancement. Besides, color vision-related genes and metabolites are proven to be correlated with myopia. This review aims to make detailed elaborations on the role of color vision in myopia and its potential interaction mechanism, hoping to provide new ideas for myopia prevention.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"254 ","pages":"Article 110324"},"PeriodicalIF":3.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143580382","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":"Loss of monocyte chemoattractant protein-1 reduced monocyte recruitment and preserved retinal ganglion cells in a mouse model of hypertensive glaucoma","authors":"Michelle Guo,&nbsp;Turner D. Schwartz,&nbsp;Emily C.N. Lawrence,&nbsp;Jingwen Lu,&nbsp;Anny Zhong,&nbsp;Jie Wu,&nbsp;Jacob K. Sterling,&nbsp;Sergei Nikonov,&nbsp;Joshua L. Dunaief,&nbsp;Qi N. Cui","doi":"10.1016/j.exer.2025.110325","DOIUrl":"10.1016/j.exer.2025.110325","url":null,"abstract":"<div><div>Monocyte chemoattractant protein-1 (MCP-1)/CCL2, a potent chemokine for myeloid cells, has been associated with disease progression in glaucoma. We examined whether genetic knockout (KO) of MCP-1 affected RGC density and function, retinal myeloid cell density, and pro-inflammatory cytokine expression in the setting of microbead induced hypertensive glaucoma. Adult wildtype (WT) C57BL/6J or MCP-1 KO mice received bilateral injections of either magnetic microbeads to elevate intraocular pressure (IOP) or balanced salt solution (BSS) as normotensive controls. After 8 weeks, immunolabeling of retina flat mounts for RBPMS and Iba1 quantified RGC and myeloid soma density in the retina, respectively. Axon density was quantified in optic nerve thin sections, while <em>in vitro</em> multi-electrode array recordings characterized RGC function. Quantitative PCR assessed expression of pro-inflammatory cytokines C1q, IL-1α, and TNF-α in macrophage/microglia-enriched retinal cellular populations. Results demonstrated lower RGC soma and axon density, and higher myeloid cellular density, in bead vs. BSS-injected eyes of WT mice. In contrast, RGC soma and axon density, as well as myeloid cellular density did not differ between bead and BSS-injected eyes of MCP-1 KO mice. Aspects of RGC firing rates were also preserved in KO compared to WT mice after IOP elevation. Interestingly, expressions of C1q, IL-1α, and TNF-α, cytokines previously shown to be cytotoxic to RGCs, did not differ between WT and KO mice. In summary, genetic ablation of MCP-1 rescued RGCs and decreased myeloid density in the retina without altering pro-inflammatory cytokine expression, supporting a pathogenic role for monocyte recruitment in hypertensive glaucoma.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"254 ","pages":"Article 110325"},"PeriodicalIF":3.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regeneration of retinal ganglion cell-like cells and reconstruction of visual neural circuits in mice with glaucoma","authors":"Zhenhao Zhang ,&nbsp;He Wang ,&nbsp;Wei Li ,&nbsp;Ya Liu ,&nbsp;Lin Xu ,&nbsp;Jianjun Liu","doi":"10.1016/j.exer.2025.110327","DOIUrl":"10.1016/j.exer.2025.110327","url":null,"abstract":"<div><div>Glaucoma is an irreversible blinding eye disease characterized by apoptosis of mature neurons-retinal ganglion cells (RGCs), visual field defect and vision loss. Regeneration of RGCs and reconstruction of the neural connections between the retina and the brain is considered an effective strategy to promote visual restoration in patients with glaucoma. However, there are currently no effective methods for regenerating RGCs to restore vision in clinical practice. Microglia are a type of glial cells that regulate the immune response in the retina and central nervous system (CNS), whether they have pluripotency and be reversed into RGCs remains unclear and challenging. This study revealed that the ectopic expression of multiple genes (<em>Brn3b</em>, <em>Sox2</em>, <em>Cbln1</em>, and <em>NP1</em>, referred to as <em>BSCN</em>) in microglia can promote their conversion into RGC-like cells by microglia fate lineage tracing <em>in vivo</em>. The regenerated RGC-like cells project axons to the distant brain and reconstruct the visual neural circuit, restoring the impaired vision in adult mice with acute glaucoma induced by retinal ischemia–reperfusion (I/R) injury. Furthermore, the regenerated RGC-like cells could survive stably for up to one year, and the same regeneration strategy was performed in older mice with acute glaucoma, which confirmed the effectiveness of the <em>BSCN</em> reprogramming to regenerate RGC-like cells. In summary, we have identified the microglia as a new type of reprogramming seed cells, and four key genes were found to be involved in regenerating RGC-like cells to restore vision. These findings highlight a new strategy of RGC-like cell regeneration and provide a theoretical basis for treatment of glaucoma in the future.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"254 ","pages":"Article 110327"},"PeriodicalIF":3.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585232","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}