Experimental eye research最新文献

{"title":"Characterization of corneal and retinal changes in a metabolic syndrome model in young and adult mice","authors":"Óscar Vivanco-Rojas ,&nbsp;Eleazar Ramírez-Hernández ,&nbsp;Edgar Zenteno ,&nbsp;Beatriz Buentello-Volante ,&nbsp;Fátima Sofía Magaña-Guerrero ,&nbsp;Alfredo Domínguez-López ,&nbsp;Emmanuel Segura-Pérez ,&nbsp;José Luis Sánchez-Salgado ,&nbsp;Mohamed Alí Pereyra-Morales ,&nbsp;Yonathan Garfias","doi":"10.1016/j.exer.2025.110496","DOIUrl":"10.1016/j.exer.2025.110496","url":null,"abstract":"<div><h3>Introduction</h3><div>Metabolic syndrome (MetS) is a cluster of metabolic abnormalities, such as central obesity, insulin resistance, dyslipidemia, and hypertension. One of the main characteristics of MetS is the presence of a chronic proinflammatory state, which activates the nuclear factor of activated T cells 5 (NFAT5) in response to the hyperosmolar state.</div></div><div><h3>Methodology</h3><div>A MetS model was generated in C57BL/6 mice fed to a high-sucrose diet for 120 days. Subsequently, clinical and biochemical parameters were evaluated to confirm MetS. Microvascular changes, histological analysis and the presence of proteins related to NFAT5 activity in inflammation (NLRP3, capase-1) and neurodegeneration (GAP43, GFAP) were evaluated in cornea and retinal tissues.</div></div><div><h3>Results</h3><div>MetS seems to accelerate the aging process, as young individuals with MetS exhibit characteristics typically seen in normal-weight adults, causes changes in the microvasculature, increasing the <em>in vivo</em> arteriole-to-venule ratio (AVR), in addition to causing NFAT5 relocalization in the retina, which triggers an increase in the inflammasome via NLRP3/caspase-1, in addition to decreasing the presence of GAP43 and GFAP. However, in the cornea, the behavior of NFAT5 is similar, as it relocalizes, but the inflammasome is not fully expressed. Similarly, the levels of the molecules involved in the development of dry eye syndrome, AQP5 and GAP43, are decreased.</div></div><div><h3>Conclusions</h3><div>Our results revealed a close relationship between MetS and ocular alterations associated with chronic systemic inflammation, which seems to play a central role in the development of these ocular complications.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110496"},"PeriodicalIF":3.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502155","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 role of corneal nerves and neuromodulators in the immune response and healing processes of corneal infections","authors":"Kofi Asiedu","doi":"10.1016/j.exer.2025.110498","DOIUrl":"10.1016/j.exer.2025.110498","url":null,"abstract":"<div><div>The integrity of corneal nerves is essential for maintaining corneal health; however, microbial keratitis caused by Acanthamoeba, fungi, bacteria, and viruses disrupts corneal neuroimmune homeostasis. Advanced imaging of the human cornea and animal models has revealed changes in the corneal subbasal nerve plexus, even in Acanthamoeba and fungal corneal infections. Moreover, corneal nerve regeneration in microbial keratitis relies on neurotrophins, regeneration-associated genes, and nerve guidance molecules. The damage to corneal nerves in microbial keratitis seems to stem from corneal neuroimmune responses or direct pathogen effects. While neuromodulators play a role in corneal healing, the complexity of corneal neuroimmune interactions and the multifactorial nature of infections may complicate establishing definitive therapeutic protocols. Research into the pathological changes and regenerative processes in corneal nerves is ongoing, and it could significantly enhance therapeutic strategies in microbial keratitis, offering hope for better patient outcomes.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110498"},"PeriodicalIF":3.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144491089","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":"Genomic analysis of glaucoma pathogenesis due to gmds mutation in zebrafish","authors":"Muhammad T. Ameen,&nbsp;Hayley Alloway,&nbsp;Modeline N. Longjohn,&nbsp;Robert L. Gendron,&nbsp;Hélène Paradis,&nbsp;Touati Benoukraf,&nbsp;Curtis R. French","doi":"10.1016/j.exer.2025.110497","DOIUrl":"10.1016/j.exer.2025.110497","url":null,"abstract":"<div><div>Glaucoma, a major cause of irreversible blindness, is characterized by optic nerve damage and loss of retinal ganglion cells (RGC). SNPs in the <em>GDP-MANNOSE 4,6-DEHYDRATASE</em> (<em>GMDS</em>) gene have been linked to primary open-angle glaucoma (POAG) and treatment responses. The <em>GMDS</em> gene plays a critical role in fucosylation, a process essential for modifying glycoproteins and glycolipids, yet no mechanism for its role in glaucoma pathology has been described. Our study investigates the effects of <em>gmds</em> haploinsufficiency using a CRISPR/Cas9 induced mutation in zebrafish. RNA sequencing (RNAseq) analysis shows significant downregulation of stress response genes including those of the crystallin family, and increased expression of cell death genes in <em>gmds</em> heterozygous mutant eyes. These gene expression changes correlate with phenotypic alterations, including RGC layer thinning, RGC loss, and reduced optic nerve head width in adult <em>gmds</em> heterozygotes relative to wild type siblings. Our findings provide new insights into the role of <em>GMDS</em> in regulating eye function and suggests that <em>GMDS</em> may influence glaucoma risk by regulating the response to stress. This study provides a layer of functional evidence supporting the predictions made by previous GWAS findings, enhancing our understanding of the genetic basis of glaucoma. It highlights the potential of <em>GMDS</em> as a therapeutic target for mitigating glaucoma-related vision loss, opening new avenues for glaucoma research and treatment development.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110497"},"PeriodicalIF":3.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505267","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":"Olink proteomics profiling reveals metabolism-related protein biomarkers in diabetic retinopathy","authors":"Qiu-Yang Zhang ,&nbsp;Hui-Ying Zhang ,&nbsp;Qing Liu ,&nbsp;Feng-Sheng Wang ,&nbsp;Yue Zhu ,&nbsp;Si-Guo Feng ,&nbsp;Jin Yao ,&nbsp;Biao Yan","doi":"10.1016/j.exer.2025.110495","DOIUrl":"10.1016/j.exer.2025.110495","url":null,"abstract":"<div><div>Diabetic retinopathy (DR) represents a microvascular complication of diabetes mellitus that is associated with metabolic dysregulation. This study employed Olink proteomics profiling to identify novel biomarkers and elucidate the potential mechanism of DR. A total of 44 patients with DR and 44 individuals with cataracts serving as controls were enrolled in the study. Aqueous humor samples from all participants were analyzed for 92 metabolism-related proteins using the Olink® Metabolism Panel. Differential expression analysis identified 78 proteins with altered expression between the two groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of differentially expressed proteins revealed that the enriched pathways were primarily associated with blood vessel development, cellular signaling, and protein degradation. Notably, TFF2 exhibited exceptional diagnostic potential for DR with an area under the curve (AUC) of 0.9974 in receiver operating characteristic (ROC) analysis. Elevated TFF2 levels were further validated in both DR patients and a streptozotocin (STZ)-induced diabetic murine model. Functional experiments revealed that TFF2 contributed to endothelial angiogenic effects in vitro and retinal vascular dysfunction in vivo. These findings underscore the potential of TFF2 as a diagnostic biomarker for DR and offer new insights into the metabolic pathways driving DR pathogenesis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110495"},"PeriodicalIF":3.0,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340060","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":"Can interventional clinical trials be implemented in intermediate age-related macular degeneration?","authors":"Robert P. Finger","doi":"10.1016/j.exer.2025.110493","DOIUrl":"10.1016/j.exer.2025.110493","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110493"},"PeriodicalIF":3.0,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340059","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":"Application of transcriptome sequencing to identify and explore biomarkers in a rat model of optic nerve crush","authors":"Sha-sha Yu ,&nbsp;Yun Zhao ,&nbsp;Xiao-hui Zhou ,&nbsp;Hui Zhang ,&nbsp;Hai-qiang Yu ,&nbsp;Xiao-yong Yuan","doi":"10.1016/j.exer.2025.110494","DOIUrl":"10.1016/j.exer.2025.110494","url":null,"abstract":"<div><div>Traumatic optic neuropathy (TON) has a profound impact on affected individuals, yet the treatment of TON continues to present significant challenges. In this context, we aimed to explore diagnostic biomarkers and potential mechanisms underlying TON in a rat optic nerve crush (ONC) model via a transcriptomics approach. We extracted total RNA from 32 rat retina samples. First, candidate genes and hub genes were identified. The biomarkers were subsequently identified by random forest (RF) and receiver operating characteristic (ROC) analyses. A nomogram was constructed to assess the diagnostic value of the biomarkers. Finally, functional analysis, subcellular localization analysis, drug prediction, and gene expression verification were performed. IFIT3, IFI44, USP18, ZBP1, IRGM, and OAS1B were identified as biomarkers in the ONC model and exhibited strong diagnostic utility, with all areas under the curve (AUCs) exceeding 0.8. Furthermore, these biomarkers were found to be collectively involved in “cytokine–cytokine receptor interactions”. Subcellular localization analysis revealed the predominant presence of these biomarkers in the cell nucleus and cytoplasm. Moreover, 8 drugs targeting OAS1B and 25 drugs targeting IRGM were predicted. Notably, the shared targeting of lipopolysaccharides, carbon nanotubes, pentachlorophenol, and silver by both OAS1B and IRGM has significant therapeutic potential. Additionally, IFIT3, IFI44, USP18, ZBP1, IRGM, and OAS1B expression levels were markedly elevated in ONC samples compared with control samples, underscoring their relevance as promising biomarkers for ONC. Therefore, we conclude that IFIT3, IFI44, USP18, ZBP1, IRGM, and OAS1B were identified as biomarkers of ONC, providing a potential theoretical basis for ONC related studies.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110494"},"PeriodicalIF":3.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330672","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":"Quercetin diminishes scleral ER stress and protein misfolding: High throughput transcriptome analysis in form-deprivation myopia of Guinea pigs","authors":"Lingfeng Lv ,&nbsp;Danyang Che ,&nbsp;Zewei Zhang ,&nbsp;Weijie Zhang ,&nbsp;Qimin Zhou ,&nbsp;Fang Li ,&nbsp;Jibo Zhou","doi":"10.1016/j.exer.2025.110485","DOIUrl":"10.1016/j.exer.2025.110485","url":null,"abstract":"<div><div>This study aims to verify the involvement of scleral endoplasmic reticulum stress (ERS) in form-deprived myopia (FDM) model of guinea pigs, investigate the therapeutic effects of quercetin (Qcn) on FDM as well as explore the underlying mechanisms in human scleral fibroblast (HSF). Scleral tissue of the right eyes of NC/FDM guinea pigs were collected for RNA-seq. Then, the animals were divided into NC/Qcn/FDM/FDM + Qcn group. After 4 weeks of treatment, qPCR analysis detected mRNA expression of ERS-related genes. Sirius red staining and Tunel staining were performed to observe collagen change and level of apoptosis in sclera. In vitro, HSF was treated with quercetin or tunicamycin (Tm). Western blotting detected expression of ERS-related molecules protein, MMP-2 and COL1A1 protein, while qPCR analysis detected mRNA expression. Level of misfolded protein and GRP78 in HSF were observed by immunofluorescence. The results came out that ERS-related genes GRP78, CHOP, ATF3 and ERS-related pathway were significantly upregulated in FDM eyes according to RNA-seq, which was confirmed by qPCR. Quercetin significantly inhibited FDM progression but did not affect normal refractive and axial development. Quercetin reduced the levels of ERS-related genes in FDM eyes, inhibited apoptosis and restored type I collagen expression. In HSF, quercetin inhibited Tm-induced ERS and reduced the accumulation of misfolded proteins. Our study pioneered the confirmation of the role of scleral ERS in FDM through RNA-seq. Quercetin mitigates FDM, likely by promoting proper protein folding, inhibiting the PERK/ATF3 signaling pathway, and alleviating ERS-induced apoptosis in HSFs.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110485"},"PeriodicalIF":3.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336444","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":"Exosomal miR-146a derived from human umbilical cord mesenchymal stem cells alleviates inflammation and apoptosis in dry eye disease by targeting SQSTM1","authors":"Lirong Chen ,&nbsp;Cao Gu ,&nbsp;Yaling Yang ,&nbsp;Taiwen He ,&nbsp;Qi Zhang","doi":"10.1016/j.exer.2025.110490","DOIUrl":"10.1016/j.exer.2025.110490","url":null,"abstract":"<div><div>Dry eye disease negatively impacts the quality of life of many patients worldwide, and currently, there is no cure. Stem cell therapy may offer a potential new treatment option. Mesenchymal stem cells (MSCs)-derived exosomes have similar effects as MSCs but with fewer side effects. This study investigated the effects and mechanisms of human umbilical cord mesenchymal stem cells (HUCMSCs)-derived exosomes in cell and mouse models of dry eye disease. Exosomes were isolated from HUCMSCs (HUCMSCs-EXO) and characterized by measuring surface markers. Human corneal epithelial cells (HCECs) were cultured in hypertonic (500 mOsm) or isotonic medium (310 mOsm) and treated with HUCMSC-EXO or PBS. A mouse model of dry eye disease was generated by treating mice with benzalkonium chloride and confirmed by measuring tear secretion and performing H&amp;E staining. Cell viability, apoptosis, RNA, and protein expression levels were assessed using CCK-8 assay, TUNEL staining, qPCR, and Western blotting. The regulation of SQSTM1 expression by miR-146a was evaluated using a dual luciferase reporting assay. Exposure to hyperosmotic pressure decreased cell viability, increased apoptosis and inflammation, decreased miR-146a expression, and increased SQSTM1 expression in HCECs. Treatment with HUCMSCs-EXO alleviated the effects of hyperosmotic pressure on inflammation and apoptosis. Overexpression of miR-146a increased cell viability and inhibited apoptosis and inflammation, suggesting that miR-146a mediates the beneficial effects of HUCMSCs-EXO. These findings were validated in the mouse model of dry eye disease. Further experiments revealed that miR-146a targets and promotes SQSTM1 expression. Overexpression of SQSTM1 increased cell viability and inhibited apoptosis and inflammation in HCECs. In conclusion, this study demonstrated that HUCMSCs-derived exosomal miR-146a targets SQSTM1 and promotes its expression, resulting in the alleviation of inflammation and apoptosis in cell and mouse models of dry eye disease.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110490"},"PeriodicalIF":3.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144483688","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 m6A transferase METTL3 regulates high glucose-induced proliferation and apoptosis of human lens epithelial cells through the lncRNA TUG1/KHSRP/p38MAPK signaling axis","authors":"Yuxuan Li,&nbsp;Ziyi Yao,&nbsp;Xiaoqin Gao,&nbsp;Yaxin Niu,&nbsp;Ziqing Gao,&nbsp;Shengqun Jiang","doi":"10.1016/j.exer.2025.110492","DOIUrl":"10.1016/j.exer.2025.110492","url":null,"abstract":"<div><div>Diabetic cataract (DC) is one of the ocular complications in diabetic patients. This study aimed to investigate the mechanism of Methyltransferase-like 3 (METTL3)/Long non-coding RNA taurine-upregulated gene 1 (lncRNA TUG1)/KH-type splicing regulatory protein (KHSRP)/p38 mitogen-activated protein kinase (p38MAPK) signaling axis in DC progression. The expression of METTL3, TUG1, KHSRP, p38, and apoptosis-related proteins in tissues and cells were detected by RT-qPCR or Western blot. The m6A level was quantified using m6A colorimetric assay. RNA immunoprecipitation (RIP) assay verified the binding between RNA and protein. Proliferation and apoptosis of human lens epithelial cells (HLECs) were analyzed by CCK8 assay and flow cytometry. High glucose (HG) increased METTL3-mediated m6A methylation, which increased TUG1 expression. Knockdown of TUG1 increased HG-induced cell proliferation and decreased apoptosis. Knockdown of TUG1 decreased KHSRP expression, and RIP assays showed that TUG1 bound to KHSRP. Knockdown of KHSRP reversed the decrease in cell proliferation and increase in apoptosis caused by TUG1 expression. KHSRP affects the phosphorylation level of p38 and regulates cell proliferation and apoptosis through the p38MAPK pathway. This suggests that the m6A transferase METTL3 regulates DC proliferation and apoptosis through the lncRNA TUG1/KHSRP/p38MAPK signaling axis, providing a novel target for the treatment of DC.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110492"},"PeriodicalIF":3.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322189","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":"TLR4 signal inhibition alleviates alkali-burn induced corneal neovascularization","authors":"Cong Xia ,&nbsp;Yan Deng ,&nbsp;Yichen Lu ,&nbsp;Lumei Kang ,&nbsp;Xiaojuan Wan ,&nbsp;Hongping Chen ,&nbsp;Xiaolong Yin","doi":"10.1016/j.exer.2025.110486","DOIUrl":"10.1016/j.exer.2025.110486","url":null,"abstract":"<div><div>Toll-like receptor 4 (TLR4), recognized as a fundamental mediator of inflammatory signaling, plays a crucial role in orchestrating the inflammatory response. Previous studies suggested that TLR4 knockout (KO) notably reduced corneal vascular areas induced by silver nitrate burn based on the morphological observation. The current study seeks to elucidate the influence of TLR4 signaling on corneal neovascularization (CNV) and to examine the underlying mechanisms. The model of alkali burn (AB)-induced CNV was built using TLR4 KO and wildtype (WT) mice. CNV was detected using a slit lamp. Corneal thickness was evaluated using H&amp;E staining. The expression levels of VEGF-A, MyD88, and NF-κB were evaluated employing Western blot analysis, immunohistochemistry, and Real-time PCR techniques. The inflammation factors, IL-1β, TNF-α, and IL-6, were quantified using Real-time PCR. In addition, Resatorvid (Tak242), a specific inhibitor of TLR4, was used to treat AB cornea of WT mice. AB enhanced TLR4 signaling components, including MyD88 and NF-κB. TLR4 inhibition alleviated AB-induced corneal neovascularization and corneal thickness. The TLR4 signal, inflammatory factors and VEGF-A were also down-regulated. Our data indicated that TLR4 participated in the pathology of AB-induced CNV. TLR4 was over-expressed in the cornea of AB mice. TLR4 inhibition alleviated AB-induced CNV, and suppressed MyD88, NF-κB, VEGF-A, and inflammation factors. These findings may provide new insights for the clinical treatment of AB-induced CNV.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110486"},"PeriodicalIF":3.0,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316258","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}