Cellular reprogramming最新文献

Photobiomodulation-Mediated Modulation of TGF-β/Smad Signaling in Stem Cell-Driven Osteogenesis. 光生物调节介导的TGF-β/Smad信号在干细胞驱动的成骨过程中的调节。

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-10-14 DOI: 10.1177/21524971261497225

Sharon Chioma Agommuo, Brendon Roets, Anine Crous

{"title":"Photobiomodulation-Mediated Modulation of TGF-β/Smad Signaling in Stem Cell-Driven Osteogenesis.","authors":"Sharon Chioma Agommuo, Brendon Roets, Anine Crous","doi":"10.1177/21524971261497225","DOIUrl":"https://doi.org/10.1177/21524971261497225","url":null,"abstract":"Bone regeneration remains a significant clinical challenge as a result of limitations presented by autografts, allografts, and synthetic implants. Mesenchymal stem cells (MSCs) serve as key drivers of osteogenesis as they can differentiate into osteoblasts and osteocytes. This process is, however, regulated by the transforming growth factor-beta (TGF-β) signaling pathway, which can upregulate the Runt-related transcription factor 2 (RUNX2) to promote early proliferation and commitment through canonical Smad signaling, and also inhibit late-stage differentiation to prevent excessive matrix deposition. These responses are refined further by noncanonical pathways. Photobiomodulation (PBM), a noninvasive light-based therapy, has emerged as a promising modulator of stem cell-driven osteogenesis, as it can interact with the TGF-β/Smad pathway. PBM exerts effects on the mitochondria, activating cytochrome c oxidase, increasing ATP production, and generating reactive oxygen species in a controlled manner. This leads to a stimulation of MSC proliferation, migration, and osteogenic differentiation. Emerging evidence from various studies shows that PBM can also modulate TGF-β/Smad signaling by activating latent TGF-β, enhancing Smad phosphorylation, and modulating the noncanonical pathways. However, evidence examining this interaction specifically during MSC osteogenesis are few, and the mechanisms underlying their interaction are incompletely understood. This review, therefore, critically examines existing evidence to elucidate some of these mechanisms for MSC osteogenesis. Although it is promising, challenges still exist in standardizing PBM parameters and conducting targeted studies in clinically relevant three-dimensional models. A clearer understanding of these interactions could provide a basis for future research aimed at advancing noninvasive regenerative strategies for bone defects and osteoporosis.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"21524971261497225"},"PeriodicalIF":2.7,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Generation of an Induced Pluripotent Stem Cell Line from a Patient with Infantile Liver Failure Syndrome 2 Carrying a Compound Heterozygous Mutation in NBAS. 携带NBAS复合杂合突变的婴儿肝衰竭综合征2患者诱导多能干细胞系的产生

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-10-14 DOI: 10.1177/21524971261497947

Bingxin Jiang, Yixuan Song, Lianhu Yu, Yizhong Wang, Ting Zhang

引用次数: 0

Liquid-Cell Interactions in the Tumor Microenvironment: Mechanisms, Biomarkers, and Therapeutic Opportunities. 肿瘤微环境中的液-细胞相互作用：机制、生物标志物和治疗机会。

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-10-01 Epub Date: 2026-05-26 DOI: 10.1177/21524971261453859

Yaou Wang, Kexin Zhang, Yujie Ma, Zhenghui Tian, Chengxia Kan, Fang Han, Xiaodong Sun

{"title":"Liquid-Cell Interactions in the Tumor Microenvironment: Mechanisms, Biomarkers, and Therapeutic Opportunities.","authors":"Yaou Wang, Kexin Zhang, Yujie Ma, Zhenghui Tian, Chengxia Kan, Fang Han, Xiaodong Sun","doi":"10.1177/21524971261453859","DOIUrl":"10.1177/21524971261453859","url":null,"abstract":"Tumor-associated fluids, including interstitial, vascular, and lymphatic fluids, are increasingly recognized as active regulators of cancer progression rather than passive transport media within the tumor microenvironment. As an integrative working concept, liquid-cell interactions describe how these fluids regulate biochemical signaling, extracellular vesicle trafficking, metabolite exchange, and force transmission among cancer, stromal, and immune cells. Hydrodynamic forces, chemical gradients, extracellular vesicles (EVs), and damage-associated signals jointly shape proliferation, invasion, metabolic reprogramming, angiogenesis, immune escape, and inflammatory propagation. Perturbations in flow, viscosity, pH, and fluid composition further remodel tissue architecture and reprogram cell states, thereby influencing therapeutic response. Clinically, liquid-phase biomarkers, including circulating cytokines, nucleic acids, EVs, and circulating tumor cells, support early detection, real-time monitoring, and resistance prediction. Therapeutically, strategies that normalize fluid dynamics, modulate soluble signaling networks, or block vesicle trafficking show translational promise and may enhance standard treatments. This review synthesizes recent advances from mechanisms to clinical applications and highlights the liquid phase as a distinct regulatory dimension of the tumor microenvironment with diagnostic and therapeutic relevance.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"126-136"},"PeriodicalIF":2.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Ferroptosis-Targeted Strategies to Counter Hypoxia- and Acidosis-Associated Immunosuppression in the Tumor Microenvironment. 肿瘤微环境中抗缺氧和酸中毒相关免疫抑制的铁中毒靶向策略

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-10-01 DOI: 10.1177/21524971261493449

Wanqiu Zhang, Xiaofei Zhang, Silin Kong, Xiaodong Sun, Kexin Zhang

{"title":"Ferroptosis-Targeted Strategies to Counter Hypoxia- and Acidosis-Associated Immunosuppression in the Tumor Microenvironment.","authors":"Wanqiu Zhang, Xiaofei Zhang, Silin Kong, Xiaodong Sun, Kexin Zhang","doi":"10.1177/21524971261493449","DOIUrl":"10.1177/21524971261493449","url":null,"abstract":"Immunotherapy has transformed cancer treatment, yet its efficacy in solid tumors remains constrained by primary or acquired resistance. Increasing evidence suggests that ferroptosis sensitivity is shaped not only by tumor intrinsic metabolic programs but also by the surrounding microenvironment. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, can directly damage tumor cells and modulate immunity through the release of danger signals and oxidized lipid mediators. At the same time, hypoxia and extracellular acidification, two common features of solid tumors, often reduce ferroptosis susceptibility by reinforcing antioxidant defenses, altering lipid composition, and weakening immune effector function. This review discusses how hypoxia, acidosis, ferroptosis tolerance, and immunosuppression intersect across solid tumors. We summarize the core metabolic and signaling mechanisms involved, compare tumor-specific patterns, and discuss therapeutic strategies that may restore ferroptosis sensitivity, improve immune activity, or both. We also highlight major translational barriers, including spatial heterogeneity, toxicity, limited biomarkers, and the need to distinguish established evidence from emerging concepts. A more precise understanding of the ferroptosis-microenvironment interface may help refine combination strategies for solid tumor immunotherapy.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"21524971261493449"},"PeriodicalIF":2.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reprogramming Stars #29: It Takes Muscle: Exploring Myogenic Reprogramming for Regenerative Medicine-An Interview with Dr. Ori Bar-Nur. 重编程明星#29：它需要肌肉：探索再生医学的肌原性重编程——对奥里·巴尔·努尔博士的采访。

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-10-01 Epub Date: 2026-08-13 DOI: 10.1177/21524971261477143

Ori Bar-Nur, Mariana Lopes, Carlos-Filipe Pereira

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ROCK Inhibition Accelerates Mesenchymal-to-Epithelial Transition and Improves Early Survival During Human Fibroblast Reprogramming. ROCK抑制加速间充质细胞向上皮细胞转变，提高人类成纤维细胞重编程的早期存活率。

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-10-01 Epub Date: 2026-08-31 DOI: 10.1177/21524971261484998

Mahsa Azhdari, Samaneh Dehghan, Ali Ghamari, Reza Mirshahi, Alireza Shoae-Hassani

{"title":"ROCK Inhibition Accelerates Mesenchymal-to-Epithelial Transition and Improves Early Survival During Human Fibroblast Reprogramming.","authors":"Mahsa Azhdari, Samaneh Dehghan, Ali Ghamari, Reza Mirshahi, Alireza Shoae-Hassani","doi":"10.1177/21524971261484998","DOIUrl":"10.1177/21524971261484998","url":null,"abstract":"The low efficiency in the production of induced pluripotent stem cell (iPSC) remains a major barrier to the widespread reprogramming applications in regenerative medicine and drug screening. Small molecules that modulate key signaling pathways offer a promising approach to overcome the reprogramming limitation. Here, we demonstrated that Thiazovivin (TZV), a selective Rho-associated coiled-coil kinase inhibitor, significantly increased human fibroblast reprogramming rate by approximately 1.4-fold (*p < 0.01). Treatment with TZV during the early phase of reprogramming enhanced colony formation, improved cell survival, and promoted the mesenchymal-to-epithelial transition (MET). Quantitative Real Time Polymerase Chain Reaction (RT-PCR) analysis revealed the downregulation of mesenchymal markers (N-cadherin, 52%; vimentin, 61%; p < 0.05) and upregulation of epithelial markers (E-cadherin, 165%; EpCAM, 95%; p < 0.05). Flow cytometry confirmed elevated expression of NANOG and TRA-1-60 pluripotency markers. Collectively, these findings suggest that TZV facilitates reprogramming through MET, offering a simple and effective strategy to enhance the efficiency and scalability of human iPSC generation.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"137-142"},"PeriodicalIF":2.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Reprogramming Stars #30: From Blood Origin to Immunoengineering-An Interview with Dr. Rio Sugimura. 重编程之星#30：从血液起源到免疫工程——采访b里约热内卢Sugimura博士。

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-09-30 DOI: 10.1177/21524971261494393

Rio Sugimura, Mariana Lopes, Carlos-Filipe Pereira

引用次数: 0

In Vitro Cellular Dynamics of Skin-Derived Fibroblasts of an MSTN^-/-Gene-Edited Buffalo. MSTN-/-基因编辑水牛皮肤源性成纤维细胞的体外细胞动力学

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-09-30 DOI: 10.1177/21524971261492151

Anushka Verma, Priyanka Singh, Gaurav Tripathi, Shavi Verma, Rashi Vasisth, Shweta Yadav, Mayank Attri, Manoj Kumar Singh, Naresh L Selokar

{"title":"In Vitro Cellular Dynamics of Skin-Derived Fibroblasts of an MSTN-/-Gene-Edited Buffalo.","authors":"Anushka Verma, Priyanka Singh, Gaurav Tripathi, Shavi Verma, Rashi Vasisth, Shweta Yadav, Mayank Attri, Manoj Kumar Singh, Naresh L Selokar","doi":"10.1177/21524971261492151","DOIUrl":"https://doi.org/10.1177/21524971261492151","url":null,"abstract":"Fibroblasts are widely used cell type in cellular reprogramming studies, including genetic engineering, due to their easy accessibility and cellular plasticity. The present work aimed to study the in vitro cellular dynamics of fibroblasts derived from an MSTN-/- (myostatin knockout) gene-edited buffalo. Established MSTN-/- fibroblasts exhibited higher cell and nuclear size, reduced doubling time, and shortened telomere length compared with wild-type cells. Assessment of mitochondrial function using JC-1 and MitoSOX dyes revealed preserved mitochondrial membrane potential; however, MSTN-/- fibroblasts showed a higher proportion of MitoSOX-positive cells, suggesting elevated mitochondrial reactive oxygen species production, potentially associated with altered cellular morphology such as vacuolation. Epigenetic profiling demonstrated significantly reduced levels of active histone acetylation marks H3K18ac and H4K5ac in MSTN-/- fibroblasts, while the repressive mark H3K9me2 remained unchanged. To evaluate their translational potential, MSTN-/- fibroblasts were used as donor cells for somatic cell nuclear transfer. In vitro developmental competence, including cleavage rates, blastocyst production rates, and total blastocyst cell number, was comparable to cloned embryos derived from wild-type cells. Overall, MSTN-/- fibroblasts display distinct cellular and epigenetic features with normal SCNT embryo production, supporting their utility for cellular reprograming studies.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"21524971261492151"},"PeriodicalIF":2.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Zfp462 Regulates the Pluripotency of Embryonic Stem Cells by Cooperating with the Core Transcriptional Network. Zfp462通过与核心转录网络合作调控胚胎干细胞的多能性

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-09-18 DOI: 10.1177/21524971261489113

Meng Yu, Yi Yang, Chunlin Chen, Jiaqi Wang, Wubin Yang, Ran Yang, Yixiao Xu, Fengsheng Wang, Chen Zhang, Yangkai Zhang, Yutong Dong, Jiangjun Wang, Ruoyi Xue, Yanping Tian, Xiaoping Cui, Yan Ruan, Hongli Li, Junlei Zhang, Rui Jian

{"title":"Zfp462 Regulates the Pluripotency of Embryonic Stem Cells by Cooperating with the Core Transcriptional Network.","authors":"Meng Yu, Yi Yang, Chunlin Chen, Jiaqi Wang, Wubin Yang, Ran Yang, Yixiao Xu, Fengsheng Wang, Chen Zhang, Yangkai Zhang, Yutong Dong, Jiangjun Wang, Ruoyi Xue, Yanping Tian, Xiaoping Cui, Yan Ruan, Hongli Li, Junlei Zhang, Rui Jian","doi":"10.1177/21524971261489113","DOIUrl":"https://doi.org/10.1177/21524971261489113","url":null,"abstract":"Zinc finger PBX1-interacting protein (Zfp462/Zfpip), a vertebrate-specific C2H2-type transcription factor, plays an essential role in early embryogenesis and the maintenance of embryonic stem cell (ESC) pluripotency. While previous studies have largely focused on its repressive functions, its potential role in transcriptional activation has remained unclear. In this study, we demonstrate that Zfp462 knockout (KO) impairs ESC self-renewal and disrupts the expression of pluripotency-associated and developmental genes. Luciferase reporter assays showed that Zfp462 overexpression increased Oct4 (also known as Pou5f1) promoter activity, whereas Zfp462 KO reduced its activity, supporting a role for Zfp462 in transcriptional activation. Integrative multiomics analyses reveal that Zfp462 is functionally integrated into the ESC core pluripotency module and cooperates with Oct4, Sox2, and Nanog to activate pluripotency-associated genes. Together, these findings reveal a critical role for Zfp462 in ESC pluripotency and establish it as a novel regulator within the pluripotency gene regulatory network.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"21524971261489113"},"PeriodicalIF":2.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hematopoietic Cell Fate Reprogramming in the Context of Pathological Processes and Translational Opportunities. 造血细胞命运重编程在病理过程和转化机会的背景下。

IF 2.7 4区医学

Cellular reprogramming Pub Date : 2026-08-01 Epub Date: 2026-06-28 DOI: 10.1177/21524971261464818

Branko Cirovic

{"title":"Hematopoietic Cell Fate Reprogramming in the Context of Pathological Processes and Translational Opportunities.","authors":"Branko Cirovic","doi":"10.1177/21524971261464818","DOIUrl":"10.1177/21524971261464818","url":null,"abstract":"The hematopoietic system consists of well-characterized lineages that provide a diverse repertoire of cell subsets and highly specialized immune functions. This review summarizes the key characteristics and criteria that define hematopoietic cell fate conversion. Perturbation of lineage-specific transcription factors can enable cell fate reprogramming through transdifferentiation, dedifferentiation, or lineage diversion. Members of the CCAAT/enhancer binding protein family of transcription factors, which efficiently convert B cells into macrophages and neutrophils, serve here as a prime example for illustrating the underlying molecular processes. In addition, this review explores disease-associated phenomena, such as lineage infidelity in leukemia, and highlights novel therapeutic strategies that employ fate conversion. Controlled reprogramming systems can also serve as scalable and robust in vitro platforms for screening approaches and for dissecting functional mechanisms. Thus, hematopoietic cell fate reprogramming provides valuable insights into the specification of cellular identity and offers translational opportunities in immunity and cancer.","PeriodicalId":9708,"journal":{"name":"Cellular reprogramming","volume":" ","pages":"107-115"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0