Journal of Cellular Physiology最新文献

Induced Pluripotent Stem Cell-Derived Small-Diameter Vascular Grafts: Scaffold Design, Immune Engineering, and Clinical Translation 诱导多能干细胞衍生的小直径血管移植物：支架设计、免疫工程和临床翻译

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-09-03 DOI: 10.1002/jcp.70226

Dohee Kim, Seohyun Choo, Seunghun S. Lee

{"title":"Induced Pluripotent Stem Cell-Derived Small-Diameter Vascular Grafts: Scaffold Design, Immune Engineering, and Clinical Translation","authors":"Dohee Kim, Seohyun Choo, Seunghun S. Lee","doi":"10.1002/jcp.70226","DOIUrl":"https://doi.org/10.1002/jcp.70226","url":null,"abstract":"<div>\u0000 \u0000 <p>Small-diameter vascular grafts (≤ 6 mm) remain a critical unmet need in cardiovascular surgery, as autologous vessels are unavailable in up to 30% of patients requiring coronary or peripheral bypass. Induced pluripotent stem cells (iPSCs) have emerged as a transformative cell source for tissue-engineered vascular grafts (TEVGs), offering unlimited self-renewal, patient-specific or universal donor potential, and the capacity to generate all vascular cell lineages. Recent breakthroughs—including iPSC-derived grafts achieving 100% patency in allogeneic primate models and the first United States Food and Drug Administration (FDA) approval of an acellular tissue-engineered vessel (SYMVESS, December 2024)—signal that clinical translation is accelerating. This review provides a comprehensive synthesis of the iPSC-to-graft pipeline, encompassing vascular cell differentiation protocols, biomaterial scaffold design, immune engineering strategies for universal grafts, bioreactor maturation, preclinical evaluation, and the evolving clinical-regulatory landscape. We critically evaluate how the convergence of clustered regularly interspaced short palindromic repeats (CRISPR)-based immune editing, advanced biomaterials, and scalable manufacturing is reshaping the field toward off-the-shelf vascular grafts. Finally, we identify remaining challenges in long-term patency, thrombogenicity, and manufacturing scalability, and propose a translational roadmap for the next decade.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878408","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

Gut-Intervertebral Disc Axis: Gut Microbiome-Driven Immune-Metabolic Imbalance and Intervertebral Disc Degeneration 肠道-椎间盘轴：肠道微生物驱动的免疫代谢失衡和椎间盘退变

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-09-03 DOI: 10.1002/jcp.70222

Xinhui Cui, Wenjia Du

{"title":"Gut-Intervertebral Disc Axis: Gut Microbiome-Driven Immune-Metabolic Imbalance and Intervertebral Disc Degeneration","authors":"Xinhui Cui, Wenjia Du","doi":"10.1002/jcp.70222","DOIUrl":"https://doi.org/10.1002/jcp.70222","url":null,"abstract":"<div>\u0000 \u0000 <p>Intervertebral disc degeneration (IDD) serves as a critical structural basis for chronic low back pain, severely impairing patients' quality of life and imposing a significant socioeconomic burden. Current interventions remain largely limited to symptomatic treatments including pharmacological analgesia and surgical intervention. The recently proposed “gut–disc axis” suggests that the gut microbiome can reshape the endplate–disc microenvironment by influencing intestinal barrier integrity, microbial metabolite profiles, and host immune–metabolic status. Existing evidence indicates that dysbiosis-related increases in endotoxin load, dysregulated metabolism of short-chain fatty acids, tryptophan, and bile acids, systemic low-grade inflammation, and shifts in immune cell lineages may collectively promote nucleus pulposus cell senescence and apoptosis, matrix degradation, and endplate pathology. Mendelian randomization studies have also suggested potential causal links between certain gut microbiota and disc diseases. However, the determination of whether “microbial signals” detected within the intervertebral disc represent true colonization is currently hindered by methodological limitations, particularly low-biomass contamination. This review focuses on mechanisms through which gut microbiota influence the endplate–disc microenvironment via immune–metabolic pathways, including the LPS/TLR4/NF-κB axis, SCFAs–AhR axis, and lipid/iron metabolism, while only briefly addressing studies related to mechanical injury and surgery. Building on these insights, we integrate advances from clinical cohorts, animal models, and multiomics studies, summarize key actionable intervention nodes, and propose a preliminary patient stratification framework and validation pathway based on gut–immune–metabolic typing, providing a theoretical foundation for developing microbiome-guided disease-modifying interventions.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878421","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

RETRACTION: PCBP2 Promotes the Development of Glioma by Regulating FHL3/TGF-β/Smad Signaling Pathway 回顾：PCBP2通过调控FHL3/TGF-β/Smad信号通路促进胶质瘤的发生

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-21 DOI: 10.1002/jcp.70211

{"title":"RETRACTION: PCBP2 Promotes the Development of Glioma by Regulating FHL3/TGF-β/Smad Signaling Pathway","authors":"","doi":"10.1002/jcp.70211","DOIUrl":"https://doi.org/10.1002/jcp.70211","url":null,"abstract":"<p><b>RETRACTION:</b> J. Mao, Z. Sun, Y. Cui, N. Du, H. Guo, J. Wei, Z. Hao and L. Zheng, “PCBP2 Promotes the Development of Glioma by Regulating FHL3/TGF-β/Smad Signaling Pathway,” <i>Journal of Cellular Physiology</i> 235, no. 4 (2020): 3280-3291, https://doi.org/10.1002/jcp.29104.</p><p>The above article, published online on 06 November 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed following concerns raised by a third party. An investigation identified multiple instances of image duplication between elements presented in Figures 3b, 3c, 4c and 7c and images published in other articles, by different authors and representing a different scientific context. Four of these articles were published prior to this article. In addition, duplication was identified in Figure 6a between the TGF-β1 western blot bands and the p-Smad2 bands. The authors did not respond to requests for comment and supporting data. The editors therefore consider the results and conclusions of this article to be compromised. The authors did not respond to our notice of retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784507","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

RETRACTION: MicroRNA-374b Inhibits Cervical Cancer Cell Proliferation and Induces Apoptosis Through the p38/ERK Signaling Pathway by Binding to JAM-2 结论：MicroRNA-374b与JAM-2结合，通过p38/ERK信号通路抑制宫颈癌细胞增殖并诱导凋亡

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-20 DOI: 10.1002/jcp.70217

引用次数: 0

Expression OF Concern: Increased Autocrine Interleukin-6 Production Is Significantly Associated With Worse Clinical Outcome in Patients With Chronic Lymphocytic Leukemia 关注的表达：慢性淋巴细胞白血病患者自分泌白细胞介素-6产生增加与较差的临床结果显著相关

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-20 DOI: 10.1002/jcp.70221

引用次数: 0

Adenylyl Cyclase (ADCY) Protein Family: Molecular Mechanisms and Therapeutic Potential in Glucose and Lipid Metabolism and Feeding Regulation 腺苷酸环化酶（ADCY）蛋白家族：糖脂代谢和摄食调节的分子机制和治疗潜力

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-13 DOI: 10.1002/jcp.70216

Shaohong Wu, Yongxue Chen, Jiali Xueting Zhang, Jinshan Zhang

{"title":"Adenylyl Cyclase (ADCY) Protein Family: Molecular Mechanisms and Therapeutic Potential in Glucose and Lipid Metabolism and Feeding Regulation","authors":"Shaohong Wu, Yongxue Chen, Jiali Xueting Zhang, Jinshan Zhang","doi":"10.1002/jcp.70216","DOIUrl":"https://doi.org/10.1002/jcp.70216","url":null,"abstract":"<div>\u0000 \u0000 <p>The adenylyl cyclase (ADCY) family comprises key signal transduction enzymes that catalyze the conversion of ATP to the second messenger cyclic adenosine monophosphate (cAMP). Through the downstream cAMP–protein kinase A (PKA) signaling pathway, this family exerts central regulatory effects on glucose and lipid homeostasis. In mammals, the ADCY family consists of nine transmembrane isoforms (ADCY1–9) and one soluble isoform (ADCY10), all of which exhibit tissue‑specific distribution, distinct regulatory mechanisms, and non‑redundant functions in core metabolic organs. Compelling evidence from gene‑edited animal models, functional validation studies, and multi‑ethnic genetic association analyses has demonstrated that dysfunction of specific ADCY isoforms is closely linked to the pathogenesis of obesity, type 2 diabetes mellitus (T2DM), metabolic dysfunction‑associated steatotic liver disease (MASLD), and other metabolic disorders. This review systematically summarizes the classification, structural characteristics, and multilayered regulatory mechanisms of the ADCY family, with a particular focus on the physiological and pathological roles of its isoforms in glucose metabolism, lipid metabolism, and feeding regulation. It also discusses recent advances in ADCY‑targeted agents and highlights unresolved challenges and future directions. Particular emphasis is given to recent structural biology breakthroughs, genetic evidence from diverse populations, and isoform‑specific therapeutic strategies, with the aim of providing a theoretical basis for mechanistic research and the development of targeted therapeutics for metabolic diseases.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753812","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

Simulated Microgravity Induced Mesenchymal Stem Cell Senescence via the Activation of Cytosolic mtDNA-cGAS-STING Axis 通过激活胞质mtDNA-cGAS-STING轴模拟微重力诱导间充质干细胞衰老。

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-09 DOI: 10.1002/jcp.70220

Lei Huang, Rui Huang, Wenjun Lv, Zimeng Li, Yun Tu, Guanbin Song, Qing Luo

{"title":"Simulated Microgravity Induced Mesenchymal Stem Cell Senescence via the Activation of Cytosolic mtDNA-cGAS-STING Axis","authors":"Lei Huang, Rui Huang, Wenjun Lv, Zimeng Li, Yun Tu, Guanbin Song, Qing Luo","doi":"10.1002/jcp.70220","DOIUrl":"10.1002/jcp.70220","url":null,"abstract":"<div>\u0000 \u0000 <p>Microgravity brings various pathological changes to astronauts, which may be related to the senescence of adult stem cells. However, how microgravity affects the senescence of stem cells remains barely known. In this study, it was found that microgravity simulated by Rotating Flat Chamber induced MSC senescence and promoted the expression of cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING), and C176, a STING inhibitor, alleviated the rotating culture-induced MSC senescence. Rotating culture also promoted the cytosolic leakage of mitochondrial DNA (mtDNA), while the depletion of mtDNA inhibited cGAS-STING activation and reversed MSC senescence. Knockdown of either BAK or BAX, proteins forming pores on the mitochondrial outer membrane, suppressed mtDNA leakage, cGAS-STING activation, and MSC senescence, suggesting that BAK/BAX mediates the activation of mtDNA-cGAS-STING axis and the associated MSC senescence. Recovering mitochondrial function by Mito TEMPO inhibited the activation of mtDNA-cGAS-STING axis and reversed MSC senescence. In vivo, using rat hindlimb unloading (HU) model to simulate microgravity, it was found that inhibition of STING ameliorated MSC senescence induced by HU. Together, our study demonstrated that simulated microgravity induces MSC senescence by the activation of cytosolic mtDNA-cGAS-STING axis and indicated cGAS-STING pathway as a therapeutic target of MSC senescence under microgravity.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701394","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

Welcome to the Relaunched Journal of Cellular Physiology 欢迎来到重新启动的细胞生理学杂志。

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-06 DOI: 10.1002/jcp.70218

Paul Trevorrow, Robert J. W. Heath

引用次数: 0

Hippo Pathway Regulation and Microenvironmental Cues Governing Human MSC Transition to Cancer-Associated Fibroblasts Hippo通路调控和微环境信号调控人间充质干细胞向癌症相关成纤维细胞的转变。

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-08-05 DOI: 10.1002/jcp.70219

Pimjai Chingsuwanrote, Chanchao Lorthongpanich, Pakpoom Kheolamai, Ting Gang Chew, Chuti Laowtammathron, Sudjit Luanpitpong, Rangsun Parnpai, Surapol Issaragrisil

{"title":"Hippo Pathway Regulation and Microenvironmental Cues Governing Human MSC Transition to Cancer-Associated Fibroblasts","authors":"Pimjai Chingsuwanrote, Chanchao Lorthongpanich, Pakpoom Kheolamai, Ting Gang Chew, Chuti Laowtammathron, Sudjit Luanpitpong, Rangsun Parnpai, Surapol Issaragrisil","doi":"10.1002/jcp.70219","DOIUrl":"10.1002/jcp.70219","url":null,"abstract":"<p>Cancer-associated fibroblasts (CAFs) are key drivers of tumor progression. This study examined how three-dimensional (3D) culture, hypoxia, and cancer-derived soluble factors influence the transformation of human mesenchymal stem cells (hMSCs) into inflammatory CAFs (iCAFs). hMSCs from bone marrow, placenta, and chorion were cultured in 2D, in Matrigel-based 3D systems, under hypoxia, and with soluble factors from colon cancer cells (HT29, HCT116). 3D culture strongly induced iCAF markers (IL1α, CSF3, IL6) while reducing myofibroblastic CAF markers (CCN2, MYL9, TAGLN). Hypoxia and cancer factors further enhanced this phenotype, promoting IL1α/IL6 secretion and shifting their influence from suppressing to stimulating cancer cell growth and angiogenesis. Mechanistically, these changes were associated with YAP/TAZ down-regulation, and genetic depletion of YAP/TAZ alone was sufficient to convert hMSCs into iCAFs even in 2D culture. These findings highlight YAP/TAZ as critical regulators of hMSC-to-CAF transformation, with implications for therapeutic strategies targeting tumor stroma.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13440140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673595","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

Multiomics Profiling Identifies Blood-Based Diagnostic Markers for Sepsis 多组学分析确定脓毒症的血液诊断标志物

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-07-30 DOI: 10.1002/jcp.70213

Xin Zhang, Xiaoqing Guo, Shuai Jiang, Yanting Cao, Shuya Wang, Wentao Xie, Jiayin Tian, Yazhe Zhou, Man Wang, Hui Chang, Yang Yang

{"title":"Multiomics Profiling Identifies Blood-Based Diagnostic Markers for Sepsis","authors":"Xin Zhang, Xiaoqing Guo, Shuai Jiang, Yanting Cao, Shuya Wang, Wentao Xie, Jiayin Tian, Yazhe Zhou, Man Wang, Hui Chang, Yang Yang","doi":"10.1002/jcp.70213","DOIUrl":"https://doi.org/10.1002/jcp.70213","url":null,"abstract":"<div>\u0000 \u0000 <p>Sepsis, characterized by a rapid transition to systemic immune dysregulation and multiorgan failure, poses a formidable clinical challenge. The lack of spatiotemporally stable biomarkers severely impedes early diagnosis and risk stratification. By integrating large-scale transcriptomic profiling with machine learning algorithms, this study identified a robust three-gene diagnostic signature (TLR5, HMGB2, and C19orf59). Single-cell RNA sequencing precisely localized the sepsis-induced specific upregulation of these targets to the myeloid immune compartment, notably monocytes and neutrophils. Crucially, disease severity stratification analysis (based on SOFA scores) revealed that while TLR5 and HMGB2 excel in identifying high-risk sepsis, C19orf59 maintains highly consistent diagnostic efficacy across all clinical severity strata. To definitively validate these findings while rigorously eliminating confounding effects from surgical or environmental stress, strictly time-matched sham-controlled cecal ligation and puncture (CLP) murine models and vehicle-controlled <i>in vitro</i> models were utilized. <i>In vivo</i> results corroborated the persistent in situ upregulation of this signature across vital target organs (lung, heart, liver) and systemic circulation. Parallel <i>in vitro</i> lipopolysaccharide (LPS)-stimulated cellular models further characterized their dynamic expression, with HMGB2 exhibiting a distinct biphasic kinetic profile mechanistically characteristic of danger-associated molecular patterns (DAMPs). Finally, independent clinical validation using sepsis patient serum corroborated the translational relevance of these targets. Collectively, this systematic multidimensional evaluation establishes TLR5, HMGB2, and C19orf59 as a highly reliable diagnostic and severity-stratification panel, providing novel molecular insights into the septic pathological cascade.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148617282","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