CellsPub Date : 2025-09-09DOI: 10.3390/cells14181411
Michael Holzer, Eva Gruden, Sanja Curcic, Gerhard Cvirn, Gunther Marsche
{"title":"ApoC3 Attenuates Platelet Activation Through GPIIb/IIIa Receptor Interaction.","authors":"Michael Holzer, Eva Gruden, Sanja Curcic, Gerhard Cvirn, Gunther Marsche","doi":"10.3390/cells14181411","DOIUrl":"10.3390/cells14181411","url":null,"abstract":"<p><p>Apolipoprotein C3 (apoC3) is a key regulator of triglyceride metabolism and has emerged as a potential therapeutic target for reducing the risk of cardiovascular disease. However, its broader physiological functions are not fully understood. This study investigates the role of apoC3 in platelet function and thrombus formation. Interestingly, human apoC3 was found to rapidly inhibit platelet activation over the tested concentration range of 0.1-10 µg/mL, with significant effects observed at low concentrations and brief pre-incubation times (from 1 min). At a concentration of 10 µg/mL, apoC3 suppressed platelet activation by approximately 70% in response to ADP and by approximately 40% in response to collagen stimulation. Depleting apoC3 from human serum enhanced platelet aggregation by more than 25 % (1.28 ± 0.19 vs. vehicle), indicating an endogenous regulatory function of apoC3. Mechanistically, apoC3 binding to platelets reduced both GPIIb/IIIa activation and P-selectin expression by around 20%. ApoC3 binding to platelets increased when platelets were activated by ADP and was partially mediated by GPIIb/IIIa, implicating this integrin as a functionally relevant receptor. Taken together, these findings reveal a novel link between apoC3 and platelet biology with potential implications for thrombotic risk and vascular homeostasis.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-09DOI: 10.3390/cells14181410
Jing Zhang, Leiyan Wei, Lei Song, Xiaofang Lu, Liang Tan, Xin Li, Li Fu, Qizhi Luo, Xubiao Xie, Yizhou Zou
{"title":"Novel BCR-Targeting Fusion Proteins for Antigen-Specific Depletion of Alloreactive B Cells in Antibody-Mediated Rejection.","authors":"Jing Zhang, Leiyan Wei, Lei Song, Xiaofang Lu, Liang Tan, Xin Li, Li Fu, Qizhi Luo, Xubiao Xie, Yizhou Zou","doi":"10.3390/cells14181410","DOIUrl":"10.3390/cells14181410","url":null,"abstract":"<p><p>Donor-specific anti-HLA antibodies (DSAs) bind to donor vascular endothelial cells and mediate allograft rejection (AMR), but a clinical challenge for which targeted therapeutic options remain limited. We used a multiplexed single-antigen bead (SAB) assay to detect anti-human leukocyte antigen (HLA) antibodies. Based on the antigens which patient's antibodies aganist to, we developed bivalent HLA-Fc fusion proteins composed of HLA-derived antigenic domains and human IgG1-Fc effector regions (rA24-Fc and rB13-Fc). Specific binding and functional activity of the HLA-Fc proteins were further validated by flow cytometry, ELISA, complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) assays. Our findings demonstrate that the fusion proteins rA24-Fc and rB13-Fc significantly reduced HLA-specific antibody reactivity in vitro. Notably, rA24-Fc and rB13-Fc selectively bound to B-cell hybridomas (e.g., mouse W6/32 cells) expressing membrane immunoglobulins (BCR) which bound to the most HLA class I antigens. Importantly, rA24-Fc and rB13-Fc elicited antigen-specific, Fc-dependent elimination of the specific B-cell hybridomas. This study highlights HLA-Fc fusion proteins as a promising therapeutic strategy for the antigen-specific suppression of depletion of alloreactive B cells through dual cytotoxic mechanisms. This precision targeted to BCR of B cells approach is used to apply to the treatment of antibody-mediated rejection.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-09DOI: 10.3390/cells14181406
Félix Javier Jiménez-Jiménez, Hortensia Alonso-Navarro, Elena García-Martín, Alba Cárcamo-Fonfría, Miguel Angel Martín-Gómez, José A G Agúndez
{"title":"Oxidative Stress and Antioxidant Therapies in Friedreich's Ataxia.","authors":"Félix Javier Jiménez-Jiménez, Hortensia Alonso-Navarro, Elena García-Martín, Alba Cárcamo-Fonfría, Miguel Angel Martín-Gómez, José A G Agúndez","doi":"10.3390/cells14181406","DOIUrl":"10.3390/cells14181406","url":null,"abstract":"<p><p>The pathogenesis of Friedreich's ataxia (FRDA) remains poorly understood. The most important event is the deficiency of frataxin, a protein related to iron metabolism and, therefore, involved in oxidative stress. Studies on oxidative stress markers and gene expression in FRDA patients have yielded inconclusive results. This is largely due to the limited number of studies, small sample sizes, and methodological differences. A notable finding is the decreased activity of mitochondrial respiratory chain complexes I, II, and III, as well as aconitase, in endomyocardial tissue. In contrast, numerous studies in experimental models of FRDA (characterized by frataxin deficiency) have shown evidence of the involvement of oxidative stress in cellular degeneration. These findings include increased iron concentration, mitochondrial dysfunction (with reduced respiratory chain complex activity and membrane potential), and decreased aconitase activity. Additionally, there is the induction of antioxidant enzymes, reduced glutathione levels, elevated markers of lipoperoxidation, and DNA and carbonyl protein oxidation. The expression of NRF2 is decreased, along with the downregulation of PGC-1α. Therefore, it is plausible that antioxidant treatment may help improve symptoms and slow the progression of FRDA. Among the antioxidant treatments tested in FRDA patients, only omaveloxolone and, to a lesser extent, idebenone (particularly for cardiac hypertrophy) have shown some efficacy. However, many antioxidant drugs have shown the ability to reduce oxidative stress in experimental models of FRDA. Therefore, these drugs may be useful in treating FRDA and are likely candidates for future clinical trials. Future studies investigating oxidative stress and antioxidant therapies in FRDA should adopt a prospective, multicenter, long-term, double-blind design.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12469045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-09DOI: 10.3390/cells14181412
Samjhana Thapa, Joo Hyun Kim, Jun Yeong Jeong, Sung Sik Hur, Seung Won Lee, Yongsung Hwang
{"title":"Mechanotransduction-Mediated Expansion of Rabbit Vocal Fold Epithelial Cells via ROCK Inhibition and Stromal Cell-Derived Paracrine Signals.","authors":"Samjhana Thapa, Joo Hyun Kim, Jun Yeong Jeong, Sung Sik Hur, Seung Won Lee, Yongsung Hwang","doi":"10.3390/cells14181412","DOIUrl":"10.3390/cells14181412","url":null,"abstract":"<p><p>Therapeutic advances for vocal fold (VF) disorders are limited by the scarcity of VF-derived epithelial cells (VFEs). Despite their substantial self-renewal capability in vivo, VFEs expand for only a few passages in vitro before succumbing to growth arrest. This has led to the extensive use of alternative cellular sources that are not exposed to physiological stresses of phonation. To address this, we developed an ideal culture strategy that enables long-term expansion of rabbit VFEs (rbVFEs), by utilizing Rho kinase inhibitor (ROCKi), epidermal growth factor (EGF), and mitomycin-treated STO cells or its conditioned media (STO-CM). ROCKi only could support short-term proliferation, and rbVFEs eventually underwent senescence. Further enhancement to ROCKi-containing media with EGF or STO-CM promoted sustained proliferation of rbVFEs. Mechanistically, non-self-renewing rbVFEs exhibited cytoskeletal remodeling associated with increased nuclear YAP localization, elevated focal adhesion, and higher traction forces, whereas self-renewing rbVFEs had cytoplasmic YAP retention, decreased adhesion, and reduced cellular tension. Our optimized culture strategy provides a robust supply of rbVFEs for advancing regenerative approaches in VF research.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-09DOI: 10.3390/cells14181407
Janaina Sena de Souza, Sandra Sanchez-Sanchez, Nicolas Amelinez-Robles, B S Guerra, Gisele Giannocco, Alysson R Muotri
{"title":"Trisomy 21 Disrupts Thyroid Hormones Signaling During Human iPSC-Derived Neural Differentiation In Vitro.","authors":"Janaina Sena de Souza, Sandra Sanchez-Sanchez, Nicolas Amelinez-Robles, B S Guerra, Gisele Giannocco, Alysson R Muotri","doi":"10.3390/cells14181407","DOIUrl":"10.3390/cells14181407","url":null,"abstract":"<p><p>Thyroid hormones (THs) are essential for brain development, and their dysregulation is associated with cognitive deficits and neurodevelopmental disorders. Down syndrome (DS), caused by trisomy 21, is frequently associated with thyroid dysfunction and impaired neurogenesis. Here, we investigated THs signaling dynamics during neural differentiation using human induced pluripotent stem cells (hiPSCs) derived from individuals with DS and controls. We analyzed the gene expression of key THs regulators-deiodinases, transporters, and receptors-and downstream target genes in hiPSCs, hiPSC-derived neural progenitor cells (NPCs), hiPSC-derived astrocytes, and hiPSC-derived neurons. DS-derived hiPSCs, hiPSC-derived NPCs, and hiPSC-derived neurons exhibited 2- to 7-fold increases in the gene expression of <i>DIO2</i> and 3- to 8-fold reductions in <i>DIO3</i>, alongside 1- to 3-fold downregulation of <i>THRA</i> and <i>THRB</i> isoforms. hiPSC-derived astrocytes showed a 4-fold decrease in the gene expression of <i>DIO2</i>, a 4-fold increase in <i>DIO3</i>, upregulation of <i>SLC16A10</i> (2-fold), and downregulation of <i>SLC7A5</i> (0.5-fold) and THs receptors (0.5- to 12-fold). hiPSC-derived neurons exhibited marked downregulation of the gene expression of <i>HOMER1</i> (0.5-fold), <i>GRIN3A</i> (14-fold), and <i>GRIN3B</i> (4-fold), accompanied by impaired spontaneous activity in multi-electrode array recordings. These findings reveal a robust, cell-type-specific imbalance between THs availability and signaling competence in DS hiPSC-derived neural cells, providing mechanistic insight into THs-related contributions to the function of DS hiPSC-derived neural cells and identifying potential therapeutic targets.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-09DOI: 10.3390/cells14181408
Mario García-Domínguez
{"title":"White Matter in Crisis: Oligodendrocytes and the Pathophysiology of Multiple Sclerosis.","authors":"Mario García-Domínguez","doi":"10.3390/cells14181408","DOIUrl":"10.3390/cells14181408","url":null,"abstract":"<p><p>Multiple sclerosis is a chronic, immune-mediated neurodegenerative disorder of the central nervous system, characterized by widespread demyelination, axonal injury, and progressive neurological impairment. The pathophysiology of multiple sclerosis involves complex interactions between immune cells and central nervous system resident cells, with oligodendrocytes (the myelin-producing glial cells) occupying a central role in both the disease's onset and progression. Oligodendrocyte dysfunction, including diminished regenerative capacity, heightened vulnerability to inflammatory cytokines, and increased susceptibility to oxidative stress, contributes significantly to the failure of remyelination observed in chronic multiple sclerosis lesions. Key factors such as microglial activation, T-cell-mediated cytotoxicity, and altered signaling pathways affecting oligodendrocyte progenitor cell maturation are explored in depth. Some therapeutic strategies under investigation encompass the use of pharmacological agents, cell-based interventions, and modulation of both the extracellular matrix and the immune microenvironment. Advancing our understanding of oligodendrocyte biology, along with the intrinsic and extrinsic factors that impede effective remyelination, is critical for the development of innovative, targeted therapies aimed at attenuating neurodegeneration and enhancing long-term clinical outcomes in patients with multiple sclerosis.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-09DOI: 10.3390/cells14181409
Yao Jiang, Yipeng Li, Qingpeng Shen, Xiaolong Yuan, Fei Gao, Bin Ma
{"title":"Comprehensive Characterization of Long Non-Coding RNAs in Porcine Tissues: Expression Patterns and Functional Insights During Oocyte Development.","authors":"Yao Jiang, Yipeng Li, Qingpeng Shen, Xiaolong Yuan, Fei Gao, Bin Ma","doi":"10.3390/cells14181409","DOIUrl":"10.3390/cells14181409","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are essential regulatory molecules involved in various biological processes in mammals. However, their expression patterns across multiple porcine tissues have not been systematically characterized. We analyzed 607 RNA-seq datasets derived from 14 porcine tissues, including backfat, gallbladder, heart, ileum, jejunum, kidney, longissimus dorsi, liver, lung, skeletal muscle, ovary, pituitary, skeletal muscle, and spleen. Additionally, we examined 63 single-cell RNA-seq datasets from porcine primary oocytes at five developmental stages. For comparative analysis, we included 20 human and 17 mouse oocyte RNA-seq datasets. We identified 52,798 porcine lncRNAs, with tissue-specific expression patterns most prominent in oocytes and least in skeletal muscle. Among them, 2169 were classified as housekeeping and 14,469 as tissue-specific lncRNAs. Cross-species analysis revealed that a small subset of oocyte-expressed lncRNAs is conserved in humans and mice, associated with catalytic activity and circadian regulation. Additionally, 44 lncRNAs were differentially expressed during oocyte development, implicating them in neurogenesis, vesicle transport, and protein modification. Our findings not only contribute to the growing body of knowledge regarding lncRNAs in porcine biology but also pave the way for future research aimed at elucidating their functional roles in reproductive biology and other physiological processes.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-08DOI: 10.3390/cells14171403
Yupei Ji, Zhizhong Wang, Zhenguo Cheng, Shuangshuang Lu, Nick R Lemoine, Renato Baleeiro, Louisa S Chard Dunmall, Yaohe Wang
{"title":"Ectopic HLA-II Expression in ESCC: Exploration of Its Relationship with Neoantigen Burden and Patient Survival.","authors":"Yupei Ji, Zhizhong Wang, Zhenguo Cheng, Shuangshuang Lu, Nick R Lemoine, Renato Baleeiro, Louisa S Chard Dunmall, Yaohe Wang","doi":"10.3390/cells14171403","DOIUrl":"10.3390/cells14171403","url":null,"abstract":"<p><p>Ectopic expression of human leukocyte antigen class II (HLA-II) on tumor cells correlates with anti-tumor immunity and prognosis in various cancers, but its role in esophageal squamous cell carcinoma (ESCC) remains unclear.</p><p><strong>Methods: </strong>HLA-II expression was evaluated in 34 ESCC tissue sections and a 102-sample tissue microarray (TMA) using immunohistochemistry (IHC) and in 10 ESCC cell lines via flow cytometry. Transcriptome sequencing of KYSE270, KYSE180, KYSE450, and KYSE510 was performed to investigate HLA-II regulatory mechanisms, while tumor samples from 104 ESCC patients were analyzed for neoantigen load. The prognostic significance of neoantigen burden was assessed using Cox regression.</p><p><strong>Results: </strong>HLA-II was ectopically expressed in ESCC, with positivity rates of 20.59% (34 tissues) and 25.49% (TMA). Among 10 ESCC cell lines, only KYSE270 exhibited spontaneous HLA-II expression. Transcriptome analysis revealed 1278 KYSE270-specific genes enriched in immune-related pathways (e.g., \"Cytokine-cytokine receptor interaction\"), suggesting immune-mediated HLA-II regulation. IFN-γ stimulation induced HLA-II expression in KYSE180, KYSE450, and KYSE510, indicating broader inducible HLA-II potential. In 104 patients, MHC-II-restricted neoantigen burden varied widely (0-75) and lacked direct correlation with HLA-II expression. Additionally, MHC-II-restricted neoantigen load was not significantly associated with overall survival (<i>p</i> > 0.05).</p><p><strong>Conclusion: </strong>Ectopic HLA-II expression in ESCC may influence the tumor immune microenvironment, while the prognostic value of MHC-II-restricted neoantigen burden in ESCC remains unclear, providing potential implications for immunotherapy strategies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 17","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12427808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-08DOI: 10.3390/cells14171399
Qiwei Yang
{"title":"Uncovering the Cellular and Molecular Landscape of Gynecological Disorders.","authors":"Qiwei Yang","doi":"10.3390/cells14171399","DOIUrl":"10.3390/cells14171399","url":null,"abstract":"<p><p>Gynecological disorders encompass a diverse array of conditions that affect the female reproductive system, including the uterus, ovaries, fallopian tubes, cervix, vagina, and external genitalia [...].</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 17","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12427882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145052268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellsPub Date : 2025-09-08DOI: 10.3390/cells14171405
Bijorn Omar Balzamino, Mariagrazia Severino, Concetta Cafiero, Marco Coassin, Antonio Di Zazzo, Alessandra Micera
{"title":"The Zebrafish as a Model for Ocular Translational Research: From Retinal Repair to Regeneration.","authors":"Bijorn Omar Balzamino, Mariagrazia Severino, Concetta Cafiero, Marco Coassin, Antonio Di Zazzo, Alessandra Micera","doi":"10.3390/cells14171405","DOIUrl":"10.3390/cells14171405","url":null,"abstract":"<p><p>In the last years, the zebrafish model has become a primary model system for vertebrate tissue regeneration, particularly for neurodegeneration and metabolic disease. Zebrafish (<i>Danio rerio</i>) are small freshwater teleosts valued for disease modelling, which are widely used in genetic laboratories, as a key model for studying neurodegenerative, metabolic, cardiac and dystrophic diseases, supporting the goal of identifying new therapeutic targets and approaches. Zebrafish can proliferate and produce/regenerate neurons. In response to retinal injury, zebrafish can regenerate multiple classes of retinal neurons and particularly, Müller glia-derived progenitor cells (MGPCs) can regenerate all types of neurons and restore visual function upon injury. The Jak/Stat-pathway of zebrafish retina represents one of the cell-signalling pathways involved in reprogramming Müller glia into MGPCs. In this era characterized by a revolution in experimental models and the future of omics, zebrafish might represent a suitable animal model for studying retinal degeneration and regeneration. In this context, the review is not meant to be entirely comprehensive of the zebrafish field, but it will highlight the usefulness of this model in discovering some mechanisms underlying retinal repair and regeneration.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 17","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12428511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145052143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}