Cell Proliferation最新文献

{"title":"Comparative Analysis of the Therapeutic Potential of Extracellular Vesicles Secreted by Aged and Young Bone Marrow-Derived Mesenchymal Stem Cells in Osteoarthritis Pathogenesis","authors":"Shital Wakale,&nbsp;Yang Chen,&nbsp;Antonia Rujia Sun,&nbsp;Chamikara Liyanage,&nbsp;Jennifer Gunter,&nbsp;Jyotsna Batra,&nbsp;Ross Crawford,&nbsp;Hongxun Sang,&nbsp;Indira Prasadam","doi":"10.1111/cpr.13776","DOIUrl":"10.1111/cpr.13776","url":null,"abstract":"<p>Osteoarthritis (OA), a joint disease, burdens global healthcare due to aging and obesity. Recent studies show that extracellular vesicles (EVs) from bone marrow-derived mesenchymal stem cells (BMSCs) contribute to joint homeostasis and OA management. However, the impact of donor age on BMSC-derived EV efficacy remains underexplored. In this study, we investigated EV efficacy from young BMSCs (2-month-old) in mitigating OA, contrasting them with EVs from aged BMSCs (27-month-old). The study used destabilisation of the medial meniscus (DMM) surgery on mouse knee joints to induce accelerated OA. Cartilage degeneration markers and senescence markers' expression levels were investigated in response to EV treatment. The therapeutic impact of EVs on chondrocytes under inflammatory responses was also evaluated. Despite having similar morphologies, EVs from young BMSCs markedly decreased senescence and improved chondroprotection by activating the PTEN pathway while simultaneously suppressing the upregulation of the PI3K/AKT pathways, proving to be more effective than those from older BMSCs in vitro. Furthermore, intraperitoneal injections of EVs from young donors significantly mitigated OA progression by preserving cartilage and reducing synovitis in a surgical OA model using DMM in mice. These findings highlight that donor age as a critical determinant in the therapeutic potential of BMSC-derived EVs for clinical use in OA treatment.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 4","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13776","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal Stem Cell-Derived Exosomes: A Promising Therapeutic Strategy for Age-Related Diseases.","authors":"Bohua Wei, Mengting Wei, Haonan Huang, Ting Fan, Zhichang Zhang, Xiaoyu Song","doi":"10.1111/cpr.13795","DOIUrl":"https://doi.org/10.1111/cpr.13795","url":null,"abstract":"<p><p>The global increase in the aging population has led to a concurrent rise in the incidence of age-related diseases, posing substantial challenges to healthcare systems and affecting the well-being of the elderly. Identifying and securing effective treatments has become an urgent priority. In this context, mesenchymal stem cell-derived exosomes (MSC-Exos) have emerged as a promising and innovative modality in the field of anti-aging medicine, offering a multifaceted therapeutic approach. MSC-Exos demonstrate significant potential due to their immunomodulatory and anti-inflammatory properties, their ability to inhibit oxidative stress, and their reparative effects on senescent tissues. These attributes make them valuable in combating a range of conditions associated with aging, such as cardiovascular diseases, neurodegeneration, skin aging, and osteoarthritis. The integration of exosomes with membrane-penetrating peptides introduces a novel strategy for the delivery of biomolecules, surmounting traditional cellular barriers and enhancing therapeutic efficacy. This review provides a comprehensive synthesis of the current understanding of MSC-Exos, underscoring their role as a novel and potent therapeutic strategy against the intricate challenges of age-related diseases.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13795"},"PeriodicalIF":5.9,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating Aging-Related Endometrial Dysfunction Using Endometrial Organoids","authors":"Minghui Lu,&nbsp;Yanli Han,&nbsp;Yu Zhang,&nbsp;Ruijie Yu,&nbsp;Yining Su,&nbsp;Xueyao Chen,&nbsp;Boyang Liu,&nbsp;Tao Li,&nbsp;Rusong Zhao,&nbsp;Han Zhao","doi":"10.1111/cpr.13780","DOIUrl":"10.1111/cpr.13780","url":null,"abstract":"<p>Ageing of the endometrium is a critical factor that affects reproductive health, yet its intricate mechanisms remain poorly explored. In this study, we performed transcriptome profiling and experimental verification of endometrium and endometrial organoids from young and advanced age females, to elucidate the underlying mechanisms and to explore novel treatment strategies for endometrial ageing. First, we found that age-associated decline in endometrial functions including fibrosis and diminished receptivity, already exists in reproductive age. Subsequently, based on RNA-seq analysis, we identified several changes in molecular processes affected by age, including fibrosis, imbalanced inflammatory status including Th1 bias in secretory phase, cellular senescence and abnormal signalling transduction in key pathways, with all processes been further validated by molecular experiments. Finally, we uncovered for the first time that PI3K-AKT-FOXO1 signalling pathway is overactivated in ageing endometrium and is closely correlated with fibrosis and impaired receptivity characteristics of ageing endometrium. Blocking or activation of PI3K by LY294002 or 740Y-P could attenuate the effect of ageing or accelerate dysfunction of endometrial organoids. This discovery is expected to bring new breakthroughs for understanding the pathophysiological processes associated with endometrial ageing, as well as treatment strategies to improve reproductive outcomes in women of advanced reproductive age.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 4","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13780","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP33 Regulates DNA Damage Response and Carcinogenesis Through Deubiquitylating and Stabilising p53.","authors":"Yuqi Zhu, Zixiang Chen, Kaifeng Niu, Mengge Li, Yuchun Deng, Ji Zhang, Di Wei, Jiaqi Wang, YongLiang Zhao","doi":"10.1111/cpr.13793","DOIUrl":"https://doi.org/10.1111/cpr.13793","url":null,"abstract":"<p><p>The de-ubiquitinase USP33 has been shown to possess either tumour-promoting or inhibitory effect on human cancer cells. However, all these findings are mainly based on in vitro cell culture models, and the in vivo evidence, which is more plausible to digest the functional role of USP33 in carcinogenic process, is still lacking. Here, we demonstrate that USP33 modulates DNA damage responses including cell cycle arrest and apoptosis induction through associating with p53. It directly interacts with p53 to mediate its de-ubiquitination and further  stabilisation under DNA damage condition. Depletion of USP33 induces an enhanced level of p53 ubiquitination, which de-stabilises p53 protein leading to impaired DNA damage responses. Furthermore, USP33 silencing shows either promoted or inhibited effect on cell proliferation in human cancer cells with p53 WT and mutant background, respectively. Consistently, mice with hepatocyte-specific USP33 knockout are more sensitive to nitrosodiethylamine (DEN)-induced hepatocarcinogenesis compared to wild type mice. Thus, our in vitro and in vivo evidences illustrate that USP33 possesses anti-tumour activity via regulating p53 stability and activity.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13793"},"PeriodicalIF":5.9,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CTCF Point Mutation at R567 Disrupts Mouse Heart Development via 3D Genome Rearrangement and Transcription Dysregulation","authors":"Huawei Ren,&nbsp;Hongxin Zhong,&nbsp;Jie Zhang,&nbsp;Yuli Lu,&nbsp;Gongcheng Hu,&nbsp;Weixun Duan,&nbsp;Ning Ma,&nbsp;Hongjie Yao","doi":"10.1111/cpr.13783","DOIUrl":"10.1111/cpr.13783","url":null,"abstract":"<p>CTCF plays a vital role in shaping chromatin structure and regulating gene expression. Clinical studies have associated CTCF mutations with congenital developmental abnormalities, including congenital cardiomyopathy. In this study, we investigated the impact of the homozygous CTCF-R567W (<i>Ctcf</i>\u0000 ^{\u0000 <i>R567W/R567W</i>\u0000}) mutation on cardiac tissue morphogenesis during mouse embryonic development. Our results reveal significant impairments in heart development, characterised by ventricular muscle trabecular hyperplasia and reduced ventricular cavity sizes. We also observe a marked downregulation of genes involved in sarcomere assembly, calcium ion transport, and mitochondrial function in heart tissues from homozygous mice. Furthermore, the <i>Ctcf</i>\u0000 ^{\u0000 <i>R567W/R567W</i>\u0000} mutation disrupts CTCF's interaction with chromatin, resulting in alterations to topologically associating domain (TAD) structure within specific genomic regions and diminishing crucial promoter-enhancer interactions necessary for cardiac development. Additionally, we find that the heterozygous CTCF-R567W (<i>Ctcf</i>\u0000 ^{\u0000 <i>+/R567W</i>\u0000}) mutation significantly compromises cardiac contractility in 8-week-old mice. This study elucidates the mechanism by which the CTCF-R567W mutation hampers cardiac development, underscoring the essential role of CTCF-R567 in embryonic heart development and maturation.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 4","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13783","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implication of GPRASP2 in the Proliferation and Hair Cell-Forming of Cochlear Supporting Cells.","authors":"Jing Cai, Kun Huang, Wenrui Li, Tianming Wang, Shen Yue, Zhibin Chen, Guangqian Xing, Qinjun Wei, Jun Yao, Xin Cao","doi":"10.1111/cpr.13792","DOIUrl":"https://doi.org/10.1111/cpr.13792","url":null,"abstract":"<p><p>G protein-coupled receptor-associated sorting protein 2 (GPRASP2) has been identified as the causative gene for X-linked recessive syndromic hearing loss (SHL) in our previous study. However, the role of GPRASP2 in auditory function remains unclear. The present study demonstrated that Gprasp2 overexpression in mouse organoids promoted the proliferation of supporting cells (SCs), which was mainly mediated by the Hedgehog signalling pathway. Meanwhile, GPRASP2 promoted hair cell (HC) formation from SCs via β-catenin signalling. In addition, GPRASP2 deficiency resulted in increased lysosomal degradation of SMO protein, leading to decreased expression of β-catenin and the Hedgehog pathway transcription factor GLI1. In neomycin-treated mouse cochlear explant, the smoothened agonist (SAG) recured the HC loss and further facilitated AAV-ie-Gprasp2 to promote the proliferation of SCs and formation of HCs. Our results suggested that GPRASP2 could be a potential candidate for gene therapy in the regeneration of HCs.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13792"},"PeriodicalIF":5.9,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell Multiomics Reveals TCR Clonotype-Specific Phenotype and Stemness Heterogeneity of T-ALL Cells","authors":"Songnan Sui,&nbsp;Xiaolei Wei,&nbsp;Yue Zhu,&nbsp;Qiuyue Feng,&nbsp;Xianfeng Zha,&nbsp;Lipeng Mao,&nbsp;Boya Huang,&nbsp;Wen Lei,&nbsp;Guobing Chen,&nbsp;Huien Zhan,&nbsp;Huan Chen,&nbsp;Ru Feng,&nbsp;Chengwu Zeng,&nbsp;Yangqiu Li,&nbsp;Oscar Junhong Luo","doi":"10.1111/cpr.13786","DOIUrl":"10.1111/cpr.13786","url":null,"abstract":"<p>T-cell acute lymphoblastic leukaemia (T-ALL) is a heterogeneous malignant disease with high relapse and mortality rates. To characterise the multiomics features of T-ALL, we conducted integrative analyses using single-cell RNA, TCR and chromatin accessibility sequencing on pre- and post-treatment peripheral blood and bone marrow samples of the same patients. We found that there is transcriptional rewiring of gene regulatory networks in T-ALL cells. Some transcription factors, such as <i>TCF3</i> and <i>KLF3</i>, showed differences in activity and expression levels between T-ALL and normal T cells and were associated with the prognosis of T-ALL patients. Furthermore, we identified multiple malignant TCR clonotypes among the T-ALL cells, where the clonotypes consisted of distinct combinations of the same TCR α and β chain per patient. The T-ALL cells displayed clonotype-specific immature thymocyte cellular characteristics and response to chemotherapy. Remarkably, T-ALL cells with an orphan TCRβ chain displayed the strongest stemness and resistance to chemotherapy. Our study provided transcriptome and epigenome characterisation of T-ALL cells categorised by TCR clonotypes, which may be helpful for the development of novel predictive markers to evaluate treatment effectiveness for T-ALL.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 4","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13786","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conditional Overexpression of Net1 Enhances the Trans-Differentiation of Lgr5+ Progenitors into Hair Cells in the Neonatal Mouse Cochlea","authors":"Yanqin Lin,&nbsp;Qiuyue Zhang,&nbsp;Wei Tong,&nbsp;Yintao Wang,&nbsp;Leilei Wu,&nbsp;Hairong Xiao,&nbsp;Xujun Tang,&nbsp;Mingchen Dai,&nbsp;Zixuan Ye,&nbsp;Renjie Chai,&nbsp;Shasha Zhang","doi":"10.1111/cpr.13787","DOIUrl":"10.1111/cpr.13787","url":null,"abstract":"<p>Sensorineural hearing loss is mainly caused by damage to hair cells (HC), which cannot be regenerated spontaneously in adult mammals once damaged. Cochlear Lgr5⁺ progenitors are characterised by HC regeneration capacity in neonatal mice, and we previously screened several new genes that might induce HC regeneration from Lgr5⁺ progenitors. <i>Net1</i>, a guanine nucleotide exchange factor, is one of the screened new genes and is particularly active in cancer cells and is involved in cell proliferation and differentiation. Here, to explore in vivo roles of Net1 in HC regeneration, <i>Net1</i>\u0000 ^{\u0000 <i>loxp/loxp</i>\u0000} mice were constructed and crossed with <i>Lgr5</i>\u0000 ^{\u0000 <i>CreER/+</i>\u0000} mice to conditionally overexpress (cOE) <i>Net1</i> in cochlear Lgr5⁺ progenitors. We observed a large number of ectopic HCs in <i>Lgr5</i>\u0000 ^{\u0000 <i>CreER/+</i>\u0000}\u0000 <i>Net1</i>\u0000 ^{\u0000 <i>loxp/loxp</i>\u0000} mouse cochlea, which showed a dose-dependent effect. Moreover, the EdU assay was unable to detect any EdU⁺/Sox2⁺ supporting cells, while lineage tracing showed significantly more regenerated tdTomato⁺ HCs in <i>Lgr5</i>\u0000 ^{\u0000 <i>CreER/+</i>\u0000}\u0000 <i>Net1</i>\u0000 ^{\u0000 <i>loxp/loxp</i>\u0000}\u0000 <i>tdTomato</i> mice, which indicated that <i>Net1</i> cOE enhanced HC regeneration by inducing the direct trans-differentiation of Lgr5⁺ progenitors rather than mitotic HC regeneration. Additionally, qPCR results showed that the transcription factors related to HC regeneration, including <i>Atoh1</i>, <i>Gfi1</i> and <i>Pou4f3</i>, were significantly upregulated and are probably the mechanism behind the HC regeneration induced by <i>Net1</i>. In conclusion, our study provides new evidence for the role of <i>Net1</i> in enhancing HC regeneration in the neonatal mouse cochlea.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 4","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13787","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Brain Organoids Model Abnormal Prenatal Neural Development Induced by Thermal Stimulation","authors":"Lei Xu,&nbsp;Yufan Zhang,&nbsp;Xingyi Chen,&nbsp;Yuan Hong,&nbsp;Xu Zhang,&nbsp;Hao Hu,&nbsp;Xiao Han,&nbsp;Xiao Zou,&nbsp;Min Xu,&nbsp;Wanying Zhu,&nbsp;Yan Liu","doi":"10.1111/cpr.13777","DOIUrl":"10.1111/cpr.13777","url":null,"abstract":"<p>The developing human foetal brain is sensitive to thermal stimulation during pregnancy. However, the mechanisms by which heat exposure affects human foetal brain development remain unclear, largely due to the lack of appropriate research models for studying thermal stimulation. To address this, we have developed a periodic heating model based on brain organoids derived from human pluripotent stem cells. The model recapitulated neurodevelopmental disruptions under prenatal heat exposure at the early stages, providing a paradigm for studying the altered neurodevelopment under environmental stimulation. Our study found that periodic heat exposure led to decreased size and impaired neural tube development in the brain organoids. Bulk RNA-seq analysis revealed that the abnormal WNT signalling pathway and the reduction of G2/M progenitor cells might be involved in heat stimulation. Further investigation revealed increased neural differentiation and decreased proliferation under heat stimulation, indicating that periodic heat exposure might lead to abnormal brain development by altering key developmental processes. Hence, our model of periodically heating brain organoids provides a platform for modelling the effects of maternal fever on foetal brain development and could be extended to applications in neurodevelopmental disorders intervention.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"58 2","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13777","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 Chemical Reprogramming Approach Efficiently Producing Human Retinal Pigment Epithelium Cells for Retinal Disease Therapies.","authors":"Ke Zhang, Yanqiu Wang, Qi An, Hengjing Ji, Defu Wu, Xuri Li, Lingge Suo, Chun Zhang, Xuran Dong","doi":"10.1111/cpr.13785","DOIUrl":"https://doi.org/10.1111/cpr.13785","url":null,"abstract":"<p><p>Human induced pluripotent stem cells (hiPSCs) represent a promising cell source for generating functional cells suitable for clinical therapeutic applications, particularly in the context of autologous cell therapies. However, the production of hiPSCs through genetic manipulation, especially involving oncogenes, may raise safety concerns. Furthermore, the complexity and high costs associated with hiPSCs generation have hindered their broad clinical use. In this study, we utilised a recently developed chemical reprogramming method in conjunction with a guided differentiation protocol, introducing a chemically defined strategy for generating functional human retinal pigment epithelium (RPE) cells from adipose tissue, bypassing conventional hiPSCs generation challenges. By utilising small molecule-based chemical cocktails, we reprogrammed somatic adipose cells into human chemically induced pluripotent stem cells (hCiPSCs) in a safer and more streamlined manner, entirely free from gene manipulation. Subsequent differentiation of hCiPSCs into functional RPE cells demonstrated their capability for secretion and phagocytosis, emphasising their vital role in maintaining retinal homeostasis and underscoring their therapeutic potential. Our findings highlight the transformative potential of hCiPSCs as a safer, more efficient option for personalised cell therapies, with applications extending beyond ocular disease to a wide range of medical conditions.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e13785"},"PeriodicalIF":5.9,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}