Cell Proliferation最新文献_第4页

Mechanical Force Regulates the Paracrine Function of ADSCs to Promote the Adipose-Regenerating Effects of AAM by Regulating Angiogenesis and the Inflammatory Response. 机械力调节ADSCs的旁分泌功能，通过调节血管生成和炎症反应促进AAM的脂肪再生作用

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-27 DOI: 10.1111/cpr.70045

Yining Wang, Luyu Zhang, Jiaxuan Liu, Yuchao Yang, Zhenyu Bi, Jun Ouyang

引用次数: 0

Elucidating the Role and Mechanism of Alpha-Enolase in Senescent Amelioration via Metabolic Reprogramming. α -烯醇化酶通过代谢重编程改善衰老的作用和机制。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-27 DOI: 10.1111/cpr.70049

Yun Haeng Lee, Hyunwoong Lim, Gyungmin Kim, Geonhee Jang, Myeong Uk Kuk, Ji Ho Park, Jee Hee Yoon, Yoo Jin Lee, Duyeol Kim, Byeonghyeon So, Minseon Kim, Hyung Wook Kwon, Youngjoo Byun, Joon Tae Park

{"title":"Elucidating the Role and Mechanism of Alpha-Enolase in Senescent Amelioration via Metabolic Reprogramming.","authors":"Yun Haeng Lee, Hyunwoong Lim, Gyungmin Kim, Geonhee Jang, Myeong Uk Kuk, Ji Ho Park, Jee Hee Yoon, Yoo Jin Lee, Duyeol Kim, Byeonghyeon So, Minseon Kim, Hyung Wook Kwon, Youngjoo Byun, Joon Tae Park","doi":"10.1111/cpr.70049","DOIUrl":"https://doi.org/10.1111/cpr.70049","url":null,"abstract":"Senescent cells are characterised by increased glycolysis dependence. Normalisation of glycolysis metabolism is essential for senescence amelioration. However, the mechanism of proteins involved in cellular glycolysis metabolism has not been fully elucidated. Here, we identified a candidate compound, an oxazole analogue (KB2764), that can improve senescence. To elucidate the mechanism of the KB2764, we investigated the interacting proteins. KB2764 interacted with alpha-enolase (ENO1) and pyruvate kinase M (PKM), ultimately allowing PKM to phosphorylate ENO1. KB2764 consequently increased mitochondrial ATP production and reduced reliance on glycolysis. Knockdown of the ENO1 experiment in senescent cells demonstrates that regulation of ENO1 activity is a prerequisite for recovery of mitochondrial function. Furthermore, the action of KB2764 extends its application to extend the lifespan of Caenorhabditis elegans. Taken together, our findings reveal a novel mechanism by which senescence is ameliorated through metabolic reprogramming and mitochondrial functional recovery via KB2764-mediated regulation of ENO1 protein activity.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70049"},"PeriodicalIF":5.9,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969509","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}

引用次数: 0

Intelligent Manufacturing for Osteoarthritis Organoids. 骨关节炎类器官的智能制造。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-26 DOI: 10.1111/cpr.70043

Xukun Lyu, Jian Wang, Jiacan Su

{"title":"Intelligent Manufacturing for Osteoarthritis Organoids.","authors":"Xukun Lyu, Jian Wang, Jiacan Su","doi":"10.1111/cpr.70043","DOIUrl":"https://doi.org/10.1111/cpr.70043","url":null,"abstract":"Osteoarthritis (OA) is the most prevalent degenerative joint disease worldwide, imposing a substantial global disease burden. However, its pathogenesis remains incompletely understood, and effective treatment strategies are still lacking. Organoid technology, in which stem cells or progenitor cells self-organise into miniature tissue structures under three-dimensional (3D) culture conditions, provides a promising in vitro platform for simulating the pathological microenvironment of OA. This approach can be employed to investigate disease mechanisms, carry out high-throughput drug screening and facilitate personalised therapies. This review summarises joint structure, OA pathogenesis and pathological manifestations, thereby establishing the disease context for the application of organoid technology. It then examines the components of the arthrosis organoid system, specifically addressing cartilage, subchondral bone, synovium, skeletal muscle and ligament organoids. Furthermore, it details various strategies for constructing OA organoids, including considerations of cell selection, pathological classification and fabrication techniques. Notably, this review introduces the concept of intelligent manufacturing of OA organoids by incorporating emerging engineering technologies such as artificial intelligence (AI) into the organoid fabrication process, thereby forming an innovative software and hardware cluster. Lastly, this review discusses the challenges currently facing intelligent OA organoid manufacturing and highlights future directions for this rapidly evolving field. By offering a comprehensive overview of state-of-the-art methodologies and challenges, this review anticipates that intelligent, automated fabrication of OA organoids will expedite fundamental research, drug discovery and personalised translational applications in the orthopaedic field.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70043"},"PeriodicalIF":5.9,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974446","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}

引用次数: 0

KYNA Ameliorates Hepatic Ischemia-Reperfusion Injury by Activating the Hippo Signalling Pathway via FTO-Dependent m6A Demethylation of LATS1. KYNA通过fto依赖的LATS1 m6A去甲基化激活Hippo信号通路，改善肝缺血再灌注损伤。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-25 DOI: 10.1111/cpr.70048

Wenjie Zheng, Xiaowen Wang, Haoqi Chen, Kaiming He, Xijing Yan, Yuan Zhang, Yang Yang, Peng Zhang, Wenfeng Zhu, Shuguang Zhu, Hua Li

{"title":"KYNA Ameliorates Hepatic Ischemia-Reperfusion Injury by Activating the Hippo Signalling Pathway via FTO-Dependent m6A Demethylation of LATS1.","authors":"Wenjie Zheng, Xiaowen Wang, Haoqi Chen, Kaiming He, Xijing Yan, Yuan Zhang, Yang Yang, Peng Zhang, Wenfeng Zhu, Shuguang Zhu, Hua Li","doi":"10.1111/cpr.70048","DOIUrl":"https://doi.org/10.1111/cpr.70048","url":null,"abstract":"Hepatic ischemia-reperfusion injury (HIRI) substantially influences the prognosis of liver transplant recipients. Although kynurenic acid (KYNA) has been associated with protective effects against ischemia-reperfusion injury in various organs, the precise mechanisms underlying its protective role in HIRI are not well elucidated. In this study, a 70% mouse HIRI model and an in vitro hypoxia/reoxygenation model were employed to examine the protective effects of KYNA on HIRI. In this study, we illustrate that KYNA influences the methylation status of the Hippo signalling pathway by enhancing the expression of the fat mass and obesity-associated gene (FTO). Within this pathway, large tumour suppressor kinase 1 (LATS1) is identified as a direct target of FTO. Moreover, the stability of LATS1 mRNA exhibits an inverse correlation with FTO levels and is modulated through its interaction with YTH N6-Methyladenosine RNA Binding Protein F2 (YTHDF2). The reduction in LATS1 expression facilitated Yes-associated protein (YAP) nuclear translocation, decreased hepatocyte apoptosis, and mitigated HIRI. Clinically, elevated levels of serum KYNA correlate with a diminished severity of liver injury post-transplantation. our work revealed that KYNA possesses significant clinical translational potential for the prevention of HIRI, and further exploration of its underlying mechanisms was conducted.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70048"},"PeriodicalIF":5.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967221","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}

引用次数: 0

Glutaminase-1 Mediated Glutaminolysis to Glutathione Synthesis Maintains Redox Homeostasis and Modulates Ferroptosis Sensitivity in Cancer Cells. 谷氨酰胺酶-1介导的谷氨酰胺水解至谷胱甘肽合成维持氧化还原稳态并调节癌细胞对铁中毒的敏感性。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-21 DOI: 10.1111/cpr.70036

Changsen Bai, Jialei Hua, Donghua Meng, Yue Xu, Benfu Zhong, Miao Liu, Zhaosong Wang, Wei Zhou, Liming Liu, Hailong Wang, Yang Liu, Lifang Li, Xiuju Chen, Yueguo Li

{"title":"Glutaminase-1 Mediated Glutaminolysis to Glutathione Synthesis Maintains Redox Homeostasis and Modulates Ferroptosis Sensitivity in Cancer Cells.","authors":"Changsen Bai, Jialei Hua, Donghua Meng, Yue Xu, Benfu Zhong, Miao Liu, Zhaosong Wang, Wei Zhou, Liming Liu, Hailong Wang, Yang Liu, Lifang Li, Xiuju Chen, Yueguo Li","doi":"10.1111/cpr.70036","DOIUrl":"https://doi.org/10.1111/cpr.70036","url":null,"abstract":"Glutaminase-1 (GLS1) has garnered considerable interest as a metabolic target in cancer due to its heightened involvement and activity. However, the precise fate of glutaminolysis catalysed by GLS1 in cancer cells remains elusive. We found that GLS1 knockout led to significant suppression of cancer cell proliferation, which can be reversed or partially restored by supplementation of glutamate or non-essential amino acids that can be converted into glutamate. The addition of spliceosomal KGA or GAC ameliorates cancer cell growth in vitro and in vivo, providing both simultaneously completely reverse the effect. The primary metabolic fate of glutamate produced through glutaminolysis in cancer cells is mainly used to produce glutathione (GSH) for redox homeostasis, not entering the tricarboxylic acid cycle or synthesising nucleotides. GSH monoethyl ester (GSH-MEE) effectively rescues the inhibition of cancer cell proliferation caused by GLS1 knockout. Deletion of GLS1 results in an elevation of reactive oxygen species (ROS) and malondialdehyde (MDA), a reduction of NADPH/NADP+ ratio, and an augmented susceptibility of cells to ferroptosis. Glutathione Peroxidase 4 (GPX4) and GPX1 exhibit complementary roles in redox regulation, with GLS1 knockout promoting GPX4 degradation. Pharmacological inhibition of GLS1 synergises with GPX4 inhibitor to suppress tumour growth. Dual targeting of GPX4 and GPX1 presents a potent anti-cancer strategy. This metabolic mechanism facilitates a deeper comprehension of the abnormal glutamine metabolism in cancer cells, establishing a theoretical basis for the potential clinical utilisation of GLS1 inhibitors and presenting novel perspectives for advancing combinatorial therapeutic approaches.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70036"},"PeriodicalIF":5.9,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976063","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}

引用次数: 0

Inhibition of Alkbh5 Attenuates Lipopolysaccharide-Induced Lung Injury by Promoting Ccl1 m6A and Treg Recruitment. 抑制Alkbh5通过促进Ccl1 m6A和Treg募集来减轻脂多糖诱导的肺损伤。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-20 DOI: 10.1111/cpr.70032

Hongdou Ding, Xinnan Xu, Yaoyao Zhu, Xinyu Ling, Li Xu

{"title":"Inhibition of Alkbh5 Attenuates Lipopolysaccharide-Induced Lung Injury by Promoting Ccl1 m6A and Treg Recruitment.","authors":"Hongdou Ding, Xinnan Xu, Yaoyao Zhu, Xinyu Ling, Li Xu","doi":"10.1111/cpr.70032","DOIUrl":"https://doi.org/10.1111/cpr.70032","url":null,"abstract":"This paper discussed the role of AlkB homologue 5 (Alkbh5) in the progression of lipopolysaccharide (LPS)-induced acute lung injury (ALI). LPS-induced ALI models were established in Alkbh5 knockout (KO) and knock-in (KI) mice. The m6A levels in lung tissues were analysed using m6A dot assays. The lung injury was analysed by determining ALI-related markers and histological staining. Mouse MLE12 cells were exposed to LPS for in vitro experiments, and the influence of Alkbh5 on cell viability, apoptosis and reactive oxygen species (ROS) production was analysed. RNA-seq analysis was performed to analyse gene changes upon Alkbh5 deficiency. Functions of the Alkbh5-C-C motif chemokine ligand 1 (Ccl1) cascade in ALI were further verified using the Alkbh5 antagonist DDO-2728 and a recombinant protein of Ccl1 (mCcl1). Alkbh5 was upregulated in lung tissues following LPS exposure. Alkbh5 knockout in mice mitigated LPS-induced lung injury, as indicated by reduced serum levels of lung injury markers and reduced immune cell infiltration, fibrosis and apoptosis. Conversely, Alkbh5 overexpression in mice resulted in reverse trends. In vitro, Alkbh5 knockdown in MLE12 cells enhanced cell viability while reducing cell apoptosis and ROS production. Mechanistically, Alkbh5 was found to bind to and destabilise Ccl1 mRNA, leading to increased Treg recruitment. Treatment with DDO-2728 or mCcl1 in mice increased Treg infiltration, thus improving lung tissue pathology and reducing lung injury. This study suggests that Alkbh5 is implicated in ALI progression by reducing Ccl1-mediated Treg recruitment, making it a promising target for ALI management.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70032"},"PeriodicalIF":5.9,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987315","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}

引用次数: 0

IMPDH2's Central Role in Cellular Growth and Diseases: A Potential Therapeutic Target. IMPDH2在细胞生长和疾病中的核心作用：一个潜在的治疗靶点。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-19 DOI: 10.1111/cpr.70031

Zheng Li, Yunpeng Zou, Jiayao Niu, Ying Zhang, Aohua Yang, Wenyu Lin, Jie Guo, Shuya Wang, Ronghan Liu

引用次数: 0

Deciphering Sequence Determinants of Zygotic Genome Activation Genes: Insights From Machine Learning and the ZGAExplorer Platform. 破译合子基因组激活基因的序列决定因素：来自机器学习和ZGAExplorer平台的见解。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-18 DOI: 10.1111/cpr.70039

Jixiang Xing, Siqi Yang, Yuchao Liang, Pengwei Hu, Bingjie Dai, Hanshuang Li, Yongqiang Xing, Yongchun Zuo

{"title":"Deciphering Sequence Determinants of Zygotic Genome Activation Genes: Insights From Machine Learning and the ZGAExplorer Platform.","authors":"Jixiang Xing, Siqi Yang, Yuchao Liang, Pengwei Hu, Bingjie Dai, Hanshuang Li, Yongqiang Xing, Yongchun Zuo","doi":"10.1111/cpr.70039","DOIUrl":"https://doi.org/10.1111/cpr.70039","url":null,"abstract":"The mammalian life cycle initiates with the transition of genetic control from the maternal to the embryonic genome during zygotic genome activation (ZGA), which becomes pivotal for development. Nevertheless, understanding the conservation of genes and transcription factors (TFs) that underlie mammalian ZGA remains limited. Here, we compiled a comprehensive set of ZGA genes from mice, humans, pigs, bovines and goats, including Nr5a2 and TPRX1/2. The identification of 111 homologous genes through comparative analyses was followed by the discovery of a conserved genetic coding region, suggesting potential sequence preferences for ZGA genes. Notably, an interpretable machine learning model based on k-mer core features showed excellent performance in predicting ZGA genes (area under the ROC curve [AUC] > 0.81), revealing abundant and intricate 6-base sequence specific patterns and potential binding TFs, including motifs from NR5A2 and TPRX1/2. Further analysis demonstrated that gene sequence features and epigenetic modification features play equally important roles in regulating ZGA genes. Ultimately, we developed the ZGAExplorer platform to provide an invaluable resource for screening ZGA genes. Our study unravels the sequence determinants of ZGA genes across species through multi-omics data integration and machine learning, yielding insights into ZGA regulatory mechanisms and embryonic developmental arrest.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70039"},"PeriodicalIF":5.9,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964764","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}

引用次数: 0

Revitalising Aging Oocytes: Echinacoside Restores Mitochondrial Function and Cellular Homeostasis Through Targeting GJA1/SIRT1 Pathway. 激活衰老卵母细胞：紫锥菊苷通过靶向GJA1/SIRT1通路恢复线粒体功能和细胞稳态。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-18 DOI: 10.1111/cpr.70044

Liuqing Yang, Xinle Lai, Fangxuan Lin, Nan Shi, Xinya Xu, Heng Wang, Xiaotian Li, Dan Shen, Haimo Qian, Xin Jin, Jiayi Chen, Zhongwei Huang, Xing Duan, Qin Zhang

{"title":"Revitalising Aging Oocytes: Echinacoside Restores Mitochondrial Function and Cellular Homeostasis Through Targeting GJA1/SIRT1 Pathway.","authors":"Liuqing Yang, Xinle Lai, Fangxuan Lin, Nan Shi, Xinya Xu, Heng Wang, Xiaotian Li, Dan Shen, Haimo Qian, Xin Jin, Jiayi Chen, Zhongwei Huang, Xing Duan, Qin Zhang","doi":"10.1111/cpr.70044","DOIUrl":"https://doi.org/10.1111/cpr.70044","url":null,"abstract":"As maternal age increases, the decline in oocyte quality emerges as a critical factor contributing to reduced reproductive capacity, highlighting the urgent need for effective strategies to combat oocyte aging. This study investigated the protective effects and underlying mechanisms of Echinacoside (ECH) on aging oocytes. ECH significantly improved cytoskeletal stability and chromosomal integrity, as demonstrated by restored spindle morphology and reinforced F-actin structures, essential for meiotic progression. It also preserved mitochondrial function by restoring membrane potential and dynamics, reducing ROS levels, and downregulating the DNA damage marker γ-H2AX, thereby alleviating oxidative stress and enhancing genomic stability. Furthermore, ECH promoted cellular homeostasis through modulation of lipid metabolism, autophagy and lysosomal function. Transcriptomic analyses identified GJA1 as a pivotal mediator of ECH's effects, validated through molecular docking and bio-layer interferometry. Functional studies showed that inhibiting GJA1 significantly reduced ECH's ability to enhance first polar body extrusion rates, mitochondrial function and antioxidant capacity, validating the critical role of the GJA1/SIRT1 pathway in combating oocyte aging. This study provides novel insights into the mechanisms of oocyte rejuvenation and highlights ECH as a promising therapeutic candidate for addressing age-related reproductive challenges.","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70044"},"PeriodicalIF":5.9,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981216","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}

引用次数: 0

Membraneless Organelles and Phase Separation in Tumours: Mechanisms and Prospects. 肿瘤中的无膜细胞器和相分离：机制和前景。

IF 5.9 1区生物学

Cell Proliferation Pub Date : 2025-04-11 DOI: 10.1111/cpr.70027

Hao Yang, Zhong Chu, Shuwen Han, Yuefen Pan

引用次数: 0