Cell and Bioscience最新文献

{"title":"Peptides targeting RAB11A-FIP2 complex inhibit HPIV3, RSV, and IAV replication as broad-spectrum antivirals.","authors":"Yanliang Jiang, Yongliang Zhao, Jie Deng, Xiaoyan Wu, Jian Li, Dong Guo, Ke Xu, Yali Qin, Mingzhou Chen","doi":"10.1186/s13578-025-01384-z","DOIUrl":"https://doi.org/10.1186/s13578-025-01384-z","url":null,"abstract":"<p><strong>Background: </strong>The cytoskeletal framework plays a critical role in the early stages of human parainfluenza virus type 3 (HPIV3) replication, including viral mRNA synthesis and translation. However, its contribution to later stages of infection, particularly in the context of RNA biology, is not well understood. This study focuses on the role of the cytoskeleton in viral nucleocapsid (vRNP, a ribonucleoprotein complex essential for RNA virus replication) transport, assembly, and budding, and explores the cooperative role of the small GTPase RAB11A and its effector RAB11 family interacting protein 2 (FIP2) in vRNP trafficking. These processes are crucial for respiratory RNA viruses like respiratory syncytial virus (RSV) and influenza A virus (IAV), highlighting the importance of RNA-protein interactions in viral pathogenesis.</p><p><strong>Results: </strong>Through the use of cytoskeleton-depolymerizing agents, the study identified actin microfilaments as indispensable for vRNP transport, viral assembly, and viral particle budding. It also revealed the importance of the RAB11A-FIP2 complex in these processes, which are critical for the intracellular trafficking of viral RNA. The development of peptides targeting the RAB11A-FIP2 complex led to the suppression of RAB11A function in infected cells, resulting in vRNP aggregation in the cytoplasm and reduced viral replication. The peptide YT-DRI showed strong broad-spectrum antiviral activity against HPIV3, RSV, and IAV in cellular and animal models and was effective against co-infections in vitro. The antiviral effects of YT-DRI were abolished upon deletion of RAB11A or core components of the RAB11A pathway.</p><p><strong>Conclusion: </strong>This work introduces a promising broad-spectrum antiviral strategy for respiratory tract infections by targeting the RAB11A-FIP2 complex, which regulates the transport and assembly of viral RNA. By disrupting this pathway, YT-DRI effectively inhibits the replication of multiple respiratory RNA viruses, including HPIV3, RSV, and IAV.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"50"},"PeriodicalIF":6.1,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144058290","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}

{"title":"Molecular mechanisms of endothelial-mesenchymal transition and its pathophysiological feature in cerebrovascular disease.","authors":"Huimin Jiang, Yifan Zhou, Weiyue Zhang, Hui Li, Wei Ma, Xunming Ji, Chen Zhou","doi":"10.1186/s13578-025-01393-y","DOIUrl":"https://doi.org/10.1186/s13578-025-01393-y","url":null,"abstract":"<p><p>The phenomenon of endothelial-mesenchymal transition (EndMT), a distinct subtype of epithelial-mesenchymal transition (EMT), has garnered significant attention from scholars. EndMT refers to the process whereby endothelial cells (ECs) transform into mesenchymal cells in response to various stimuli, resulting in the loss of their original characteristics. This process has diverse implications in both physiological and pathological states. Under physiological conditions, EndMT plays a crucial role in the development of the cardiovascular system. Conversely, under pathological conditions, EndMT has been identified as a pivotal factor in the development of cardiovascular diseases. Nonetheless, a comprehensive overview of EndMT in cerebrovascular disease is currently lacking. Here, we discuss the heterogeneity of EndMT occurrence and the regulatory factors involved in its development and analyze the feasibility of EndMT as a therapeutic target, aiming to provide a solid theoretical foundation and evidence to address diseases caused by pathological EndMT.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"49"},"PeriodicalIF":6.1,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036270","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}

{"title":"Nicotinamide mononucleotide promotes female germline stem cell proliferation by activating the H4K16ac-Hmgb1-Fyn-PLD signaling pathway through epigenetic remodeling.","authors":"Hong Zhou, Yujie Liu, Geng G Tian, Ji Wu","doi":"10.1186/s13578-025-01387-w","DOIUrl":"https://doi.org/10.1186/s13578-025-01387-w","url":null,"abstract":"<p><strong>Background: </strong>Nicotinamide mononucleotide (NMN), an endogenous nucleotide essential for various physiological processes, has an unclear role and regulatory mechanisms in female germline stem cell (FGSC) development.</p><p><strong>Results: </strong>We demonstrate that NMN significantly enhances FGSC viability and proliferation. Quantitative acetylation proteomics revealed that NMN markedly increases the acetylation of histone H4 at lysine 16 (H4K16ac). Subsequent chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq) identified high mobility group box 1 (Hmgb1) as a downstream target of H4K16ac, a finding further validated by ChIP-qPCR. Knockdown of Hmgb1 reduced FGSC proliferation by disrupting cell cycle progression, inducing apoptosis, and decreasing chromatin accessibility. High-throughput chromosome conformation capture (Hi-C) analysis showed that Hmgb1 knockdown induced A/B compartment switching, increased the number of topologically associating domains (TADs), and decreased chromatin loop formation in FGSCs. Notably, the chromatin loop at the promoter region of Fyn proto-oncogene (Fyn) disappeared following Hmgb1 knockdown. ChIP-qPCR and dual-luciferase reporter assays further confirmed the interaction between Hmgb1 and the Fyn promoter. Importantly, Fyn overexpression reversed the inhibitory effects of Hmgb1 knockdown on FGSC proliferation. Proteomic analysis suggested this rescue was mediated through the phospholipase D (PLD) signaling pathway, as Fyn overexpression selectively enhanced the phosphorylation of PLD1 at threonine 147 without affecting serine 561. Furthermore, treatment with 5-fluoro-2-indolyldechlorohaloamide, a PLD inhibitor, nullified the pro-proliferative effects of Fyn overexpression.</p><p><strong>Conclusions: </strong>Our findings reveal that NMN promotes FGSC proliferation by activating the H4K16ac-Hmgb1-Fyn-PLD signaling pathway through epigenetic remodeling. These results deepen our understanding of FGSC proliferation and highlight potential therapeutic avenues for advancing FGSC applications in reproductive medicine.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"48"},"PeriodicalIF":6.1,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12004683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003074","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}

{"title":"Distribution of gut microbiota across intestinal segments and their impact on human physiological and pathological processes.","authors":"Ke Yang, Guangqin Li, Qihong Li, Wei Wang, Xu Zhao, Nan Shao, Hui Qiu, Jing Liu, Lin Xu, Juanjuan Zhao","doi":"10.1186/s13578-025-01385-y","DOIUrl":"https://doi.org/10.1186/s13578-025-01385-y","url":null,"abstract":"<p><p>In recent years, advancements in metagenomics, metabolomics, and single-cell sequencing have enhanced our understanding of the intricate relationships between gut microbiota and their hosts. Gut microbiota colonize humans from birth, with their initial composition significantly influenced by the mode of delivery and feeding method. During the transition from infancy to early childhood, exposure to a diverse diet and the maturation of the immune system lead to the gradual stabilization of gut microbiota's composition and distribution. Numerous studies have demonstrated that gut microbiota can influence a wide range of physiological functions and pathological processes by interacting with various tissues and organs through the gut-organ axis. Different intestinal segments exhibit unique physical and chemical conditions, which leads to the formation of vertical gradients along the intestinal tract: aerobes and facultative aerobes mainly live in the small intestine and anaerobic bacteria mainly live in the large intestine, and horizontal gradients: mucosa-associated microbiota and lumen-associated microbiota. In this review, we systematically summarize the distribution characteristics of gut microbiota across six intestinal segments: duodenum, jejunum, ileum, cecum, colon, and rectum. We also draw a conclusion that gut microbiota distributed in different intestinal segments affect the progression of different diseases. We hope to elucidate the role of microbiota at specific anatomic sites within the gut in precisely regulating the processes of particular diseases, thereby providing a solid foundation for developing novel diagnostic and therapeutic strategies for related diseases.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"47"},"PeriodicalIF":6.1,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021841","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}

{"title":"The RBM39 degrader indisulam inhibits acute megakaryoblastic leukemia by altering the alternative splicing of ZMYND8.","authors":"Ying Yang, Zhiheng Li, Yang Yang, Peifang Xiao, Zhixu He, Zimu Zhang, Yizhen Li, Lei Shi, Xiaodong Wang, Yanfang Tao, Junjie Fan, Fenli Zhang, Chunxia Yang, Fahua Yao, Tongting Ji, Yongping Zhang, Bi Zhou, Juanjuan Yu, Ailian Guo, Zhongling Wei, Wanyan Jiao, Yumeng Wu, Yan Li, Di Wu, Yijun Wu, Li Gao, Yixin Hu, Jian Pan, Shaoyan Hu, Xiaoyan Yang","doi":"10.1186/s13578-025-01380-3","DOIUrl":"https://doi.org/10.1186/s13578-025-01380-3","url":null,"abstract":"<p><strong>Background: </strong>Acute megakaryoblastic leukemia (AMKL) is a rare hematological malignancy in adults but children. Alternative splicing (AS) has been shown to affect hematological cancer progression, making splicing factors promising targets. Our research aims to investigate the efficacy of the molecular glue degrader indisulam, which targets the splicing factor RNA binding motif protein 39 (RBM39) in AMKL models.</p><p><strong>Results: </strong>Public drug sensitivity data analysis revealed that AMKL cell lines exhibited the highest sensitivity to indisulam compared with other tumor types. Then we confirmed that RBM39 depletion by indisulam treatment induced AMKL cell cycle arrest and apoptosis. In AMKL mouse model, indisulam treatment significantly reduced the leukemic burden and prolonged the lifetime of AMKL mice. Mechanically, integration of transcriptomic and proteomic analyses revealed that indisulam-mediated RBM39 degradation resulted in AS of the transcription factor zinc finger MYND-type containing 8 (ZMYND8), an AMKL cell growth regulator. Finally, the effectiveness of indisulam depended on DDB1- and Cul4- Associated Factor 15 (DCAF15) expression because knockout of DCAF15 rescued the indisulam-induced RBM39 degradation and mis-splicing of ZMYND8.</p><p><strong>Conclusion: </strong>Indisulam is a promising therapeutic candidate for AMKL and the RBM39-mediated ZMYND8 splicing plays an important role in promoting the development of AMKL.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"46"},"PeriodicalIF":6.1,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11995665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034393","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}

{"title":"Dysregulated ac4C modification of mRNA in a mouse model of early-stage Alzheimer's disease.","authors":"Hao-Nan Ji, Hai-Qian Zhou, Jing-Bo Qie, Wen-Mei Lu, Hai-Tao Gao, Dan-Hong Wu","doi":"10.1186/s13578-025-01389-8","DOIUrl":"https://doi.org/10.1186/s13578-025-01389-8","url":null,"abstract":"<p><strong>Background: </strong>The identification and intervention of Alzheimer's Disease (AD) in its early-stage allows for the timely implementation of lifestyle modifications and therapeutic strategies. Although dysregulation of protein expression has been reported in the brain from AD patients and AD animal models, the underlying mechanisms remain poorly understood. N4-acetylcytidine (ac4C), the only known form of RNA acetylation in eukaryotes, has recently been shown to regulate mRNA stability and translation efficiency. However, the dysregulation of ac4C associated with abnormal protein expression levels in the brain of early-stage mouse models of AD remains to be elucidated.</p><p><strong>Methods: </strong>This study investigated ac4C modifications, mRNA and protein expression in the hippocampus of 3 and 6-month-old 5×FAD mice, a mouse model of AD, and wild-type (WT) littermates. The multi-omics analysis was performed: acetylated RNA immunoprecipitation followed by next-generation sequencing (acRIP-seq) to identify ac4C mRNAs, deep RNA sequencing (RNA-seq) to quantify mRNA abundance, and label-free quantitative proteomics to assess protein expression levels. In addition, we used acRIP-qPCR, regular qPCR and western blots to verify the ac4C, mRNA and protein levels of some key genes that were identified by the high-throughput assays.</p><p><strong>Results: </strong>Proteomic analysis revealed significant change of protein expression in the hippocampus of 3-months-old 5×FAD mice, compared with WT littermates. In contrast, RNA-seq analysis indicated that there were no substantial alterations in mRNA expression levels in the hippocampus of 3-months-old 5×FAD mice, compared to WT littermates. Strikingly, acRIP-seq revealed notable variations in ac4C modification on mRNAs, particularly those associated with synaptic structure and function, in the hippocampus of 3-months-old 5×FAD mice, compared with WT littermates. The ac4C modifications were found to be correlated with protein expression changes. Genes that are essential for synaptic function and cognition, including GRIN1, MAP2, and DNAJC6, exhibited reduced ac4C and protein levels in 3-months-old 5×FAD mice, without any corresponding changes in the mRNA levels, compared with WT littermates. Moreover, only a small part of dysregulated ac4C mRNAs identified in the 3-month-old 5×FAD mice were found in the 6-month-old 5×FAD mice.</p><p><strong>Conclusions: </strong>Altogether these results identified abnormal ac4C modification of mRNAs that may contribute to the dysregulation of protein synthesis in the hippocampus from an early-stage mouse model of AD.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"45"},"PeriodicalIF":6.1,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11995559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055687","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}

{"title":"Special correlation between diet and MASLD: positive or negative?","authors":"Jia Liu, Changmeng Li, Yun Yang, Jingtao Li, Xiaoguang Sun, Yinqiang Zhang, Runping Liu, Fafeng Chen, Xiaojiaoyang Li","doi":"10.1186/s13578-025-01382-1","DOIUrl":"https://doi.org/10.1186/s13578-025-01382-1","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic and systemic metabolic liver disease characterized by the presence of hepatic steatosis and at least one cardiometabolic risk factor (CMRF). The pathogenesis of MASLD involves multiple mechanisms, including lipid metabolism disorders, insulin resistance, inflammatory responses, and the hepato-intestinal axis of metabolic dysfunction. Among these factors, diet serves as both an inducement and a potential remedy in the disease's development. Notably, a high-lipid diet exacerbates fat accumulation, oxidative stress, and inflammatory responses, thereby promoting the progression of MASLD. Consequently, dietary induction models have become vital tools for studying the pathological mechanisms of MASLD, providing a foundation for identifying potential therapeutic targets. Additionally, we summarize the therapeutic effects of dietary optimization on MASLD and elucidate the role of specific dietary components in regulating the hepato-intestinal axis, lipid metabolism, and inhibiting inflammatory responses. In conclusion, studies utilizing animal models of MASLD offer significant insights into dietary therapy, particularly concerning the regulation of lipid metabolism-related and hepatoenteric axis-related signaling pathways as well as the beneficial mechanism of probiotics in hepatoenteric regulation. By understanding the specific mechanisms by which different dietary patterns affect MASLD, we can assess the clinical applicability of current dietary strategies and provide new directions for research and treatment aimed at disease modification.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"44"},"PeriodicalIF":6.1,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11992798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144046836","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}

{"title":"The influence of SARS-CoV-2 spike protein exposure on retinal development in the human retinal organoids.","authors":"Jing Gong, Lingling Ge, Yuxiao Zeng, Cao Yang, Yushan Luo, Jiahui Kang, Ting Zou, Haiwei Xu","doi":"10.1186/s13578-025-01383-0","DOIUrl":"https://doi.org/10.1186/s13578-025-01383-0","url":null,"abstract":"<p><strong>Background: </strong>Pregnant women are considered a high-risk population for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, as the virus can infect the placenta and embryos. Recently, SARS-CoV-2 has been widely reported to cause retinal pathological changes and to infect the embryonic retina. The infection of host cells by SARS-CoV-2 is primarily mediated through spike (S) protein, which also plays a crucial role in the pathogenesis of SARS-CoV-2. However, it remains poorly understood how the S protein of SARS-CoV-2 affects retinal development, and the underlying mechanism has not yet been clarified.</p><p><strong>Methods: </strong>We used human embryonic stem cell-derived retinal organoids (hEROs) as a model to study the effect of S protein exposure at different stages of retinal development. hEROs were treated with 2 μg/mL of S protein on days 90 and 280. Immunofluorescence staining, RNA sequencing, and RT-PCR were performed to assess the influence of S protein exposure on retinal development at both early and late stages.</p><p><strong>Results: </strong>The results showed that ACE2 and TMPRSS2, the receptors facilitating SARS-CoV-2 entry into host cells, were expressed in hEROs. Exposure to the S protein induced an inflammatory response in both the early and late stages of retinal development in the hEROs. Additionally, RNA sequencing indicated that early exposure of the S protein to hEROs affected nuclear components and lipid metabolism, while late-stages exposure resulted in changes to cell membrane components and the extracellular matrix.</p><p><strong>Conclusion: </strong>This work highlights the differential effects of SARS-CoV-2 S protein exposure on retinal development at both early and late stages, providing insights into the cellular and molecular mechanisms underlying SARS-CoV-2-induced developmental impairments in the human retina.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"43"},"PeriodicalIF":6.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11987193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055783","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}

{"title":"Shared and distinct peripheral blood immune cell landscape in MCTD, SLE, and pSS.","authors":"Yanling Cui, Huina Zhang, Yaxuan Deng, Orion Fan, Junbang Wang, Zhonggang Xing, Jianping Tang, Wenmin Zhu, Bangdong Gong, Yi Eve Sun","doi":"10.1186/s13578-025-01374-1","DOIUrl":"https://doi.org/10.1186/s13578-025-01374-1","url":null,"abstract":"<p><strong>Background: </strong>Mixed connective tissue disease (MCTD) is a rare autoimmune disease, and little is known about its pathogenesis. Furthermore, MCTD, systemic lupus erythematosus (SLE), and primary Sjögren's syndrome (pSS) share many clinical, laboratory, and immunological manifestations. This overlap complicates early diagnosis and accurate treatment.</p><p><strong>Methods: </strong>The transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from MCTD patients was performed using both bulk RNA sequencing and single-cell RNA sequencing (scRNA-seq) for the first time. Additionally, we applied MCTD scRNA-seq data, along with datasets from SLE (GSE135779) and pSS (GSE157278) from the Gene Expression Omnibus database, to characterize and compare the similarities and heterogeneity among MCTD, SLE, and pSS.</p><p><strong>Results: </strong>We first resolved transcriptomic changes in peripheral blood immune cells of MCTD, and then revealed the shared and unique features among MCTD, SLE, and pSS. Analyses showed that the percentage of CD8⁺ effector T cells was increased, while mucosal-associated invariant T cells were decreased in all three diseases. Genes related to the 'interferon (IFN) γ response' and 'IFN α response' were significantly upregulated. SCENIC analysis revealed activation of STAT1 and IRF7 in disease states, targeting IFN-related genes. The IFN-II signaling network was notably elevated in all three diseases. Unique features of MCTD, SLE, and pSS were also identified.</p><p><strong>Conclusion: </strong>We dissected the immune landscape of MCTD at single-cell resolution, providing new insights into the development of novel biomarkers and immunotherapies for MCTD. Furthermore, we offer insights into the transcriptomic similarities and heterogeneity across different autoimmune diseases, while highlighting prospective therapeutic targets.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"42"},"PeriodicalIF":6.1,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11983850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989451","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}

{"title":"A review of the 661W cell line as a tool to facilitate treatment development for retinal diseases.","authors":"Alicia A Brunet, Rebekah E James, Petria Swanson, Livia S Carvalho","doi":"10.1186/s13578-025-01381-2","DOIUrl":"10.1186/s13578-025-01381-2","url":null,"abstract":"<p><p>Retinal diseases encompass a diverse group of disorders that affect the structure and function of the retina, leading to visual impairment and, in some cases, irreversible vision loss. The investigation of retinal diseases is crucial for understanding their underlying mechanisms, identifying potential therapeutic targets, and developing effective treatments. The use of in vitro cell models has become instrumental in advancing our knowledge of these disorders, but given that these conditions usually affect retinal neuronal cell types, access to appropriate cell models can be potentially challenging. Among the available in vitro cell models, the 661W cone-like cell line has emerged as a valuable tool for studying various retinal diseases, ranging from monogenic conditions, such as inherited retinal diseases, to complex conditions such as age-related macular degeneration (AMD), diabetic retinopathy, amongst others. Developed from immortalized murine photoreceptor cells, and freely available for academics from its creator, the 661W cell line has offered visual scientists and clinicians around the world a reliable and well-characterised platform for investigating disease pathogenesis, exploring disease-specific molecular signatures, and evaluating potential therapeutic interventions. This review aims to provide an overview of the 661W cell line and its applications in the study of both inherited and acquired retinal diseases. By examining the applications and limitations of this unique cell line, we may gain valuable insights into its contributions in unravelling the complexities of retinal diseases and its potential impact on the development of novel treatments for these diseases.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"41"},"PeriodicalIF":6.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765658","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}