Journal of Cell Communication and Signaling最新文献

{"title":"Urinary exosomes aggravate diabetic kidney disease by inducing podocyte ferroptosis via the miR-217/SIRT1/Nrf2 pathway.","authors":"Xin Du, Yubo Jiang, Hongbin Guo, Haiying Zhang, Shaoqing Wang, Hao Deng, Xinyi Huang, Xiu Li","doi":"10.1002/ccs3.70076","DOIUrl":"10.1002/ccs3.70076","url":null,"abstract":"<p><p>Urinary exosomal microRNAs (miRNAs) mediate intercellular communication in diabetic kidney disease (DKD), a leading contributor to end-stage renal failure. However, the involvement of urinary exosomal miR-217 in DKD remains poorly understood. Urinary exosomes were characterized, and miR-217 expression was measured in clinical samples. The miR-217/SIRT1 interaction was validated by dual-luciferase assays. Podocyte viability, ferroptosis-related markers, and protein expression were assessed in vitro, whereas renal function and histology were evaluated in a streptozotocin-induced DKD mouse model. MiR-217 was upregulated in urinary exosomes derived from patients with DKD. Inhibition of miR-217 alleviated exosome-induced podocyte injury, lipid peroxidation, and ferroptosis, and preserved podocyte markers; these protective effects can be partially reversed by Fer-1 or miR-217 inhibition. SIRT1 was confirmed to be a direct target of miR-217, which negatively regulated SIRT1 expression and suppressed the SIRT1/Nrf2 pathway. SIRT1 knockdown abolished the protective effects of miR-217 inhibition. Conversely, miR-217 mimic exacerbated ferroptotic damage and downregulated the expression of podocyte markers, which were partly rescued by SIRT1 overexpression. In vivo, miR-217 inhibition attenuated DKD-exosome-aggravated kidney injury and ferroptosis, whereas SIRT1 inhibition abrogated this protective effect. Collectively, these findings indicate that urinary exosomal miR-217 promotes podocyte ferroptosis and DKD progression via suppression of the SIRT1/Nrf2 pathway, suggesting a potential therapeutic target for DKD.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 ","pages":"e70076"},"PeriodicalIF":4.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-mediated miR-4660 delivery inhibits OPN promoted hepatoma cells aggression through targeting LGALS3BP.","authors":"Cuihua Liu, Riwen An, Ting Lin, Lei Qu, Xiaopeng Zheng, Jingkun Lu, Mei Hong, Pengwei Zhao, Fangxin Zhao, Xuan Zhang","doi":"10.1002/ccs3.70073","DOIUrl":"10.1002/ccs3.70073","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is an aggressive malignant tumor with poor prognosis due to its strong metastatic potential. Studies linked osteopontin (OPN) to increased HCC metastasis. However, the mechanisms, especially those involving exosomes, are not well elucidated. This study investigates how OPN influences HCC cells behavior via exosome mediation. A stable HCC cell line overexpressing OPN, named SMMC-OPN, was established. Co-culture experiment revealed that exosomes from SMMC-OPN cells enhanced the migration and invasion of the parental SMMC-7721 cells. RNA sequencing found the downregulation of miR-4660 in these exosomes, which targets LGALS3BP (galectin-3 binding protein), elevated in both SMMC-OPN cells and their exosomes. Treatment with SMMC-OPN exosomes resulted in an upregulation of LGALS3BP expression in SMMC-7721 cells. Notably, upon forced overexpression of miR-4660 in SMMC-OPN cells, miR-4660 was observed to be encapsulated in exosomes. Co-culture experiments demonstrated that exosomes containing miR-4660, derived from miR-4660-overexpressing SMMC-OPN cells, counter-acted the promigratory and invasive effects of SMMC-OPN exosomes on recipient SMMC-7721 cells. These findings suggest that the downregulation of miR-4660 in SMMC-OPN exosomes contributes to the enhanced metastatic potential of HCC through modulating LGALS3BP. Furthermore, miR-4660 delivery via exosomes inhibits OPN-promoted hepatoma cell aggression by targeting LGALS3BP, highlighting a potential therapeutic target against cancer metastasis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":"e70073"},"PeriodicalIF":4.0,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148083571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Next-generation signaling: Powering the future of publications in the Journal of Cell Communication and Signaling","authors":"Brahim Chaqour","doi":"10.1002/ccs3.70069","DOIUrl":"10.1002/ccs3.70069","url":null,"abstract":"<p>The <i>Journal of Cell Communication and Signaling</i> (<i>JCCS</i>) is dedicated to advancing understanding of how intracellular and extracellular signaling coordinate environmental sensing, gene regulation, and tissue homeostasis and how their dysregulation or misinterpretation contributes to disease. Reflecting on my first year as editor-in-chief, I am pleased to highlight the journal's continued progress and strategic development. Submissions, readership, and article diversity have grown steadily, driven by the commitment of authors, reviewers, editors, and publishing staff. <i>JCCS</i> remains selective yet inclusive in scope, emphasizing high-quality studies that illuminate signaling processes in health and disease. Ongoing initiatives to reduce decision times and enhance the expertise and global representation of our editorial and reviewer communities reinforce peer review as a rigorous collaborative enterprise. A key milestone ahead is the transition of <i>JCCS</i> manuscript handling to Wiley's Research Exchange (REX) platform, which integrates submission, integrity screening, and peer review within a unified system. This platform leverages artificial intelligence tools, metadata extraction, and ORCID integration to improve efficiency, transparency, and ethical oversight. Looking forward, <i>JCCS</i> aims to strengthen peer review, introduce special issues on emerging topics in cell communication, and foster greater international engagement to advance the field's scientific and collaborative frontiers.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12966339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic targeting of MALT1 in oncology: Mechanism, inhibitor development, and clinical prospects","authors":"Xintao Cao,&nbsp;Peixia Wang,&nbsp;Yuan Ji,&nbsp;Yongliang Sun,&nbsp;Dejiu Zhang","doi":"10.1002/ccs3.70066","DOIUrl":"10.1002/ccs3.70066","url":null,"abstract":"<p>MALT1, a multifunctional protease molecule, plays a pivotal role in the adaptive immunity by regulating immune cell survival, proliferation and activation through the nuclear transcription factor-κB (NF-κB) signaling pathway by scaffold and protease activities. Aberrant activation of MALT1 is implicated in the pathogenesis of hematologic malignancies, particularly diffuse large B-cell lymphoma, and select solid tumors. Emerging research studies highlight MALT1 inhibitors as promising therapeutic agents for B-cell malignancies, with several candidates demonstrating preclinical and clinical efficacy. Notably, agents such as safimaltib (JNJ-67856633) have shown manageable safety profiles and preliminary antitumor activity in early-phase trials for relapsed/refractory B-cell malignancies. However, MALT1-targeted therapy poses a dual challenge: although inhibiting oncogenic signaling and tumor cell proliferation, it also disrupts immunosuppressive Treg function, risking autoimmune toxicity by compromising the tumor microenvironment. This review systematically analyzes MALT1's oncogenic roles across cancers, clarifies inhibitor mechanisms, and evaluates translational challenges and strategic opportunities for precision oncology and combination immunotherapy.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12953060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphoenolpyruvate carboxykinase 2 activation of the AMPK–CEBPB axis to enhance glutamine utilization to promote glycolysis and malignant behavior in adenocarcinomas cells under glucose deprivation","authors":"Libo Ruan,&nbsp;Kewang Xu,&nbsp;Wenjun Zeng,&nbsp;Ling Xiao,&nbsp;Minjun Zhao,&nbsp;Haiyan Zhang","doi":"10.1002/ccs3.70064","DOIUrl":"10.1002/ccs3.70064","url":null,"abstract":"<p>Glucose deprivation (Glu-D) is a critical feature of the tumor microenvironment. Under such conditions, tumor cells seek alternative metabolic resources to maintain rapid growth and proliferation. Glutamine serves as a key alternative resource for cancer cells, yet the metabolic mechanisms involving its transporters in non-small cell lung cancer remain poorly understood. Lentiviral vectors for overexpression and knockdown of phosphoenolpyruvate carboxykinase 2 (PCK2), solute carrier family 38 member 2 (SLC38A2), and CEBPB were constructed. Transwell, flow cytometry, Western blotting, and dual-luciferase reporter assays were used to investigate the regulatory relationship between PCK2 and SLC38A2 under Glu-D, as well as their effects on cellular glutamine metabolism, glycolysis, and malignant cell behaviors. PCK2 and SLC38A2 were highly expressed in human adenocarcinomas tissues. PCK2 upregulated SLC38A2 expression, though this effect was indirect. Under Glu-D, knockdown of PCK2 or SLC38A2 significantly reduced cellular glutamine utilization, inhibited glycolysis, and suppressed malignant cell behaviors. Treatment with an AMP-activated protein kinase (AMPK) inhibitor or knockdown of CEBPB produced similar effects. PCK2 activated AMPK, which increased downstream SLC38A2 expression by activating the transcription factor CEBPB. PCK2 upregulates SLC38A2 expression via the AMPK–CEBPB axis, enhancing glutamine utilization to promote glycolysis and malignant behaviors in A549 cells under Glu-D.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12948644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to Favorable and poor prognosis B-cell precursor acute lymphoblastic leukemia subtypes reveal distinct leukemic cell properties when interacting with mesenchymal stem cells, differentially modifying their cell stemness and leukemia chemoresistance","authors":"","doi":"10.1002/ccs3.70068","DOIUrl":"https://doi.org/10.1002/ccs3.70068","url":null,"abstract":"<p>Ángel Cortés, S., Rojas Zambrano, P.-M. and Vernot, J.-P. (2025), Favorable and poor prognosis B-cell precursor acute lymphoblastic leukemia subtypes reveal distinct leukemic cell properties when interacting with mesenchymal stem cells, differentially modifying their cell stemness and leukemia chemoresistance. J. Cell Commun. Signal, 19: e70009. https://doi.org/10.1002/ccs3.70009.</p><p>In the originally published article, the authors' names were included incorrectly. The correct names are mentioned below. The online version of this article has been corrected.</p><p>We apologize for this error.</p><p>Incorrect:</p><p>Ángel Cortés Santiago, Rojas Zambrano Paula-Manuela, Vernot Jean-Paul</p><p>Correct:</p><p>Santiago Ángel Cortés, Paula-Manuela Rojas Zambrano, Jean-Paul Vernot</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147288505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural maintenance of chromosome protein 1A exacerbates liver fibrosis by enhancing hepatic stellate cell activation and extracellular matrix synthesis via laminin subunit gamma 2 activation","authors":"Dandan Wang,&nbsp;Ning Li,&nbsp;Ranyan Gao,&nbsp;Jiaxin Wang,&nbsp;Lingyi Xu,&nbsp;Fengchun Li,&nbsp;Xinyu Geng,&nbsp;Ram Prasad Chaulagain,&nbsp;Babalola Deborah Oluwaseun,&nbsp;Xiaoyu Zhang,&nbsp;Shuang Jin,&nbsp;Shizhu Jin","doi":"10.1002/ccs3.70067","DOIUrl":"10.1002/ccs3.70067","url":null,"abstract":"<p>Liver fibrosis is characterized by an abnormal buildup of extracellular matrix (ECM), which is primarily produced by hepatic stellate cells (HSCs). Laminin subunit gamma 2 (LAMC2) is an ECM protein whose functional role in hepatic fibrosis remains to be fully elucidated. Herein, we examine how LAMC2 contributes to liver fibrosis and explore the molecular mechanisms in both animal and cellular models. LAMC2 was knocked down in C57BL/6J mice with CCl4-induced liver fibrosis. Rescue experiments were conducted in sh-LAMC2-treated and recilisib (PI3K/Akt agonist)-treated mice. The transcription factors associated with LAMC2 in liver fibrosis were predicted and verified. Transforming growth factor (TGF)-β1-stimulated LX-2 cells (HSC line) were infected with lentiviral vectors for in vitro assays. LAMC2, which was enriched in the PI3K/Akt pathway, was increased in the liver tissues of mice treated with CCl4, and recilisib reversed LAMC2 knockdown-mediated alleviation of liver fibrosis in these mice. LAMC2 transcription in activated HSCs was caused by structural maintenance of chromosome protein 1A (SMC1A). The inhibitory effect of SMC1A knockdown on ECM accumulation and HSC activation was mitigated by LAMC2 overexpression. This study provides new insights and highlights the promising potential of the SMC1A/LAMC2/PI3K/Akt axis as a therapeutic target for liver fibrosis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease","authors":"Matthias B. Moor,&nbsp;Mikhail Burmakin,&nbsp;Anna Levin,&nbsp;Gül Gizem Korkut,&nbsp;David Brodin,&nbsp;Annika Wernerson,&nbsp;Annette Bruchfeld,&nbsp;Peter Bárány,&nbsp;Anna Witasp,&nbsp;Jaakko Patrakka,&nbsp;Hannes Olauson","doi":"10.1002/ccs3.70061","DOIUrl":"https://doi.org/10.1002/ccs3.70061","url":null,"abstract":"<p>FGF23 excess is associated with morbidity and mortality, but the role of excessive circulating FGF23 concentrations as a causative factor of pathology is controversial. Here, we investigated the consequences of FGF23 excess in kidney disease. This study used three disease models: anti-glomerular basement membrane (anti-GBM) disease, Adriamycin nephropathy, and adenine-containing diets. Anti-GBM and Adriamycin mice and matched control mice received recombinant FGF23 (1 µg) or vehicle for six days (anti-GBM) or once (Adriamycin model), with dissection 24 h after the last injection. We established precision-cut kidney slices (PCKS) in adenine nephropathy for 24 h of treatment with recombinant FGF23 or vehicle. We assessed serum cytokines, biochemistry, and renal transcriptomes and histology of mice and patients with IgA nephropathy. RNA-Seq data and published transcriptomes underwent gene set enrichment, bulk ligand–receptor interaction analysis, and cell-type decomposition. Experimental anti-GBM disease caused decreased glomerular filtration rate, albuminuria, and renal tubular casts. FGF23 treatment increased phosphaturia and circulating soluble tumor necrosis factor receptor 1. The anti-GBM model showed FGF23-driven proinflammatory transcriptional signatures and Vcam1, Pdgfrb, and chemokine signaling, which were absent in FGF23-treated healthy mice. FGF23 increased renal macrophage content by transcriptome deconvolution and by immunofluorescence. In Adriamycin-induced nephropathy and in PCKS from adenine nephropathy, short-term FGF23 excess increased proinflammatory transcripts. Human data revealed associations between circulating FGF23 and renal immune cell infiltration. We found FGF23-driven renal patterns of proinflammatory gene and protein expression or leukocyte overabundance. The present data provide evidence that excess FGF23 directly drives inflammation in kidney disease and may serve as a therapeutic target.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70061","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147288444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Extracellular vesicle-LncRNA HOTAIR modulates esophageal cancer chemoresistance and immune microenvironment via miR-375/CDH2 pathway”","authors":"","doi":"10.1002/ccs3.70065","DOIUrl":"10.1002/ccs3.70065","url":null,"abstract":"<p>Tuersong, T., Shataer, M., Chen, Y., Chen, G., Li, X., Lei, L., Younusi, A. and Ma, L. (2025), Extracellular vesicle-LncRNA HOTAIR modulates esophageal cancer chemoresistance and immune microenvironment via miR-375/CDH2 pathway. <i>J. Cell Commun. Signal</i>, 19: e70014. https://doi.org/10.1002/ccs3.70014.</p><p>In the originally published article, author Tayier Tuersong's affiliations were given incorrectly. The correct affiliations are shown below. The online version of this article has been corrected.</p><p>Incorrect:</p><p>Tayier Tuersong¹, Munire Shataer², Yan Chen¹, Gaosi Chen³, Xiaoling Li¹, Linjie Lei¹, Ayiguli Younusi¹, Liangying Ma¹</p><p>¹Department of Pharmacy, Xinjiang Key Laboratory of Neurological Diseases, Xinjiang Clinical Research Center for Nervous System Diseases, Second Affiliated Hospital of Xinjiang Medical University, Urumqi, China</p><p>²Department of Histology and Embryology, Basic Medical College of Xinjiang Medical University, Urumqi, China</p><p>³Department of Nephrology, Wuhan Children's Hospital, Wuhan Maternal and Child Healthcare Center, Tongji Medical College, Huazhong University of Science &amp; Technology, Wuhan, China</p><p>Correct:</p><p>Tayier Tuersong^1,2, Munire Shataer³, Yan Chen¹, Gaosi Chen⁴, Xiaoling Li¹, Linjie Lei¹, Ayiguli Younusi¹, Liangying Ma¹</p><p>¹State Key Laboratory of Pathogenesis, Prevention and Treatment of High-Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, China</p><p>²Department of Pharmacy, Xinjiang Key Laboratory of Neurological Diseases, Xinjiang Clinical Research Center for Nervous System Diseases, Second Affiliated Hospital of Xinjiang Medical University, Urumqi, China</p><p>³Department of Histology and Embryology, Basic Medical College of Xinjiang Medical University, Urumqi, China</p><p>⁴Department of Nephrology, Wuhan Children's Hospital, Wuhan Maternal and Child Healthcare Center, Tongji Medical College, Huazhong University of Science &amp; Technology, Wuhan, China</p><p>We apologize for this error.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}