Journal of Cellular Physiology最新文献

筛选
英文 中文
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-07
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148067941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-04
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148065367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-04
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148066338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-04
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148066337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-04
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148065286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Cell Mechanics in Cancer: Integrating Mechanotransduction Pathways Within the Tumor Microenvironment. 肿瘤细胞力学:整合肿瘤微环境中的机械转导途径。
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-01 DOI: 10.1002/jcp.70184
Merve Sevgi, Yağmur Işık, Caner Karaca, Esmahan Çağlar, Hasan Berkay Abdioğlu, Ferican Zendel, Yasemin Başbınar, Hüseyin Üvet
{"title":"Cell Mechanics in Cancer: Integrating Mechanotransduction Pathways Within the Tumor Microenvironment.","authors":"Merve Sevgi, Yağmur Işık, Caner Karaca, Esmahan Çağlar, Hasan Berkay Abdioğlu, Ferican Zendel, Yasemin Başbınar, Hüseyin Üvet","doi":"10.1002/jcp.70184","DOIUrl":"10.1002/jcp.70184","url":null,"abstract":"<p><p>Single-cell mechanical properties such as stiffness, elasticity, and viscosity, are crucial in governing biological processes like migration, proliferation, and differentiation. In cancer, the mechanical properties of cells undergo significant alterations, which contribute to tumor growth, metastasis, and resistance to therapy. This review focuses on cancer cell stiffness and explores how its regulation is disrupted by the complex interplay among cytoskeletal remodeling, nuclear mechanics, and extracellular matrix (ECM) interactions. Cancer-associated fibroblasts (CAFs) and ECM composition within the tumor microenvironment (TME) modulate cellular mechanics via mechanotransduction pathways involving Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) and integrin-focal adhesion kinase (FAK) signaling. Increasing evidence supports cell stiffness as a promising diagnostic and prognostic biomarker, as well as a predictor of treatment response. Therefore, advanced techniques for measuring cell stiffness such as atomic force microscopy (AFM), Brillouin microscopy, and acousto-holography are evaluated with a focus on their potential clinical applicability. However, translation into routine oncology practice remains limited by technical variability, lack of standardized protocols, and the need for large-scale clinical validation. This review highlights the potential of integrating biomechanical markers into clinical workflows as a means to advance cancer diagnostics and enable more personalized therapeutic strategies.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70184"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13159791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868627","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}
引用次数: 0
Hematopoietic Stem Cell Tropism Mediated Targeting of Breast Cancer Stem Cells via Alteration of Tumor Immune-Microenvironment. 造血干细胞趋向性通过肿瘤免疫微环境的改变介导乳腺癌干细胞靶向。
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-01 DOI: 10.1002/jcp.70179
Sumit Mallick, Siddhartha Biswas, Sudheer Shenoy P, Bipasha Bose
{"title":"Hematopoietic Stem Cell Tropism Mediated Targeting of Breast Cancer Stem Cells via Alteration of Tumor Immune-Microenvironment.","authors":"Sumit Mallick, Siddhartha Biswas, Sudheer Shenoy P, Bipasha Bose","doi":"10.1002/jcp.70179","DOIUrl":"10.1002/jcp.70179","url":null,"abstract":"<p><p>The ontogenic development of hematopoietic stem cells (HSCs) occurs across diverse niches, with HSCs migrating from the aorta-gonad-mesonephros (AGM) to the fetal liver and finally residing in the bone marrow after birth, where adult HSCs replenish the hematopoietic system. The HSC niche critically regulates tropism and proliferation via factors secreted by the microenvironment interaction. Here, we hypothesized that HSCs display tropism toward the aggressive cancer stem cell (CSC) niches of triple-negative breast cancer (TNBC) and MCF-7 cells breast cancer, which exhibit high relapse rates and are potential targets for cell therapy. Our results demonstrate HSC-specific tropism toward breast CSCs, leading to interactions that trigger HSC differentiation into CD4<sup>+</sup> and CD8<sup>+</sup> subpopulations within the cancer microenvironment. Proteomics of migrated HSCs toward TNBC-CSCs/MCF-7 cells revealed significant upregulation of IL-7, Notch, and other proteins involved in T cell activation and migration pathways. Metabolomics of HSC-conditioned medium (HSC-CM)-treated CSCs/MCF-7 cells further demonstrated that HSC-CM arrests TNBC-CSC growth and cell cycle progression by altering the mitochondrial bioenergetics. This study highlights the potential of leveraging both HSCs and HSC-derived factors for personalized therapies targeting CSCs in TNBC.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70179"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Connexin Regulation and Modulation of Neural Stem Cell Differentiation Induced by Cell-Permeable Itaconate. 细胞渗透性衣康酸诱导神经干细胞分化的连接蛋白调控。
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-01 DOI: 10.1002/jcp.70185
Simona Denaro, Simona Rosa Spina, Simona D'Aprile, Anna Gervasi, Filippo Torrisi, Carmela Parenti, Agata Zappalà, Nunzio Vicario, Rosalba Parenti
{"title":"Connexin Regulation and Modulation of Neural Stem Cell Differentiation Induced by Cell-Permeable Itaconate.","authors":"Simona Denaro, Simona Rosa Spina, Simona D'Aprile, Anna Gervasi, Filippo Torrisi, Carmela Parenti, Agata Zappalà, Nunzio Vicario, Rosalba Parenti","doi":"10.1002/jcp.70185","DOIUrl":"10.1002/jcp.70185","url":null,"abstract":"<p><p>Neural stem cells (NSCs) are multipotent cells of the central nervous system (CNS) capable of self-renewal, differentiation, and responding to and shaping the surrounding microenvironment. Their continuous crosstalk with surrounding CNS cells is a key component of their therapeutic potential, particularly in tissue repair and regeneration. Communication in the CNS relies on complementary mechanisms, including connexins (Cxs)-based intercellular communication, to maintain homeostasis and coordinate responses to physiological and pathological stimuli. Itaconate, an endogenous shunt product of the tricarboxylic acid cycle, functions as an immunometabolite involved in inflammation and oxidative stress and has recently been implicated in neuroimmune modulation. Although itaconate influences several signalling cascades and is exchanged between cells and/or released into the extracellular milieu, its effects on Cxs expression in NSCs and whether the modulation of Cxs expression profile represents a driving factor in shaping cell fate remain unclear. Here, we investigated the effect of dimethyl itaconate, a cell-permeable esterified itaconate derivative, on the expression profile of Cxs in NSCs and its potential to modulate NSCs fate and differentiation. We found that dimethyl itaconate modulates Cxs expression in NSCs, increasing Cx36 levels, and promotes NSCs differentiation toward a neuronal phenotype, while inhibition of Cxs-based channels with carbenoxolone or mefloquine abolishes these dimethyl itaconate-induced effects. Collectively, these findings highlight a regulatory role for cell-permeable itaconate and contribute to the understanding of intercellular communication in the CNS microenvironment, providing insights into potential therapeutic strategies for CNS repair and regeneration.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70185"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13159055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868557","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}
引用次数: 0
Ginsenoside-Rh2 Alleviates Pyroptosis of Nucleus Pulposus Cells by Activating Autophagy via HIF-1α to Retard the Progression of Intervertebral Disc Degeneration. 人参皂苷- rh2通过HIF-1α激活髓核细胞自噬,减缓椎间盘退变进程,减轻髓核细胞焦亡。
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-01 DOI: 10.1002/jcp.70189
Jun Xuan, Jian Chen, Huawei Liu, Yi Chen, Zhiguang Zhang
{"title":"Ginsenoside-Rh2 Alleviates Pyroptosis of Nucleus Pulposus Cells by Activating Autophagy via HIF-1α to Retard the Progression of Intervertebral Disc Degeneration.","authors":"Jun Xuan, Jian Chen, Huawei Liu, Yi Chen, Zhiguang Zhang","doi":"10.1002/jcp.70189","DOIUrl":"10.1002/jcp.70189","url":null,"abstract":"<p><p>In the pathogenesis of intervertebral disc degeneration (IVDD), nucleus pulposus (NP) cell dysfunction is a pivotal factor, specifically manifested as extracellular matrix degradation, impaired autophagy, and pyroptosis. Ginsenoside-Rh2 (GRh2) possesses pharmacological activities, yet its role in IVDD remains unclear. This study used interleukin-1β (IL-1β) to mimic the pathological state of IVDD in vitro: GRh2 restored NP cell viability, alleviated extracellular matrix damage, repaired autophagic function, and inhibited pyroptosis. Through network pharmacology and molecular docking, HIF-1α was identified as a key functional pathway; blocking HIF-1α with BAY872243 completely abolished the aforementioned effects of GRh2. In rat IVDD models, GRh2 maintained disc structural stability and extracellular matrix homeostasis, while BAY872243 reversed this protective effect. In conclusion, GRh2 alleviates IVDD by activating autophagy mediated by HIF-1α, as well as inhibiting pyroptosis and extracellular matrix damage, making it a potential therapeutic agent for IVDD.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70189"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
The ABHD10-KCMF1 Complex Mitigates Cochlear Aging by Regulating Mitochondrial Lipid Metabolism. ABHD10-KCMF1复合物通过调节线粒体脂质代谢减轻耳蜗老化。
IF 4 2区 生物学
Journal of Cellular Physiology Pub Date : 2026-05-01 DOI: 10.1002/jcp.70193
Lu Peng, Xingwei Liao, Ying Liu, Chunqin Qiu, Zhenzhen Tang, Zhanrong Huang, Hongxiang Liao, Shihua Yin
{"title":"The ABHD10-KCMF1 Complex Mitigates Cochlear Aging by Regulating Mitochondrial Lipid Metabolism.","authors":"Lu Peng, Xingwei Liao, Ying Liu, Chunqin Qiu, Zhenzhen Tang, Zhanrong Huang, Hongxiang Liao, Shihua Yin","doi":"10.1002/jcp.70193","DOIUrl":"10.1002/jcp.70193","url":null,"abstract":"<p><p>Presbycusis is caused by multiple factors, the mechanisms of which are not fully understood. This study investigated mitochondria-related genes in presbycusis, a condition with multifactorial and incompletely understood mechanisms, by combining Mendelian randomization analysis and functional validation. Genetically predicted higher ABHD10 expression was identified as a protective factor against presbycusis and was regulated by methylation sites such as cg15684481, whereas methylation at other sites inhibited ABHD10 expression and alleviated the condition. In contrast, ABHD10 was upregulated in d-galactose-induced HEI-OC1 cells and aged mouse cochlear hair cells, where it promoted senescence. Silencing ABHD10 in senescent cells reduced P21 and P16 protein levels, decreased reactive oxygen species levels, improved mitochondrial membrane potential, and lowered lipid droplet formation along with triglycerides and fatty acids. Co-immunoprecipitation experiments showed that ABHD10 interacts with KCMF1, indicating that the complex may regulate cellular metabolism and stress responses through signaling pathways. This was supported by GO and KEGG analyses linking ABHD10 to aging-related processes such as energy metabolism and oxidative stress. Overall, ABHD10 functions as a context-dependent mitochondrial regulator, with the ABHD10-KCMF1 axis integrating mitochondrial quality control, lipid homeostasis, and redox balance, thereby offering a potential druggable target for presbycusis.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70193"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书