EUROPEAN JOURNAL OF CELL BIOLOGY欧洲细胞生物学杂志
EUROPEAN JOURNAL OF CELL BIOLOGY(英文缩写 EUR J CELL BIOL),ISSN 0171-9335,eISSN 1618-1298,中文译名:欧洲细胞生物学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.020 | Q2 |
| 2022 | 6.600 | Q2 |
| 2023 | 4.500 | Q2 |
| 2024 | 4.300 | Q2 |
| 2025 | 4.300 | Q2 |
EUROPEAN JOURNAL OF CELL BIOLOGY 最新收录文献
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1. Design and synthesis of reagents for generation and characterization of high-affinity antibodies for a Staphylococcus aureus serotype 8 disaccharide.
PMID:日期:2026-09-12Staphylococcus aureus is a common, opportunistic pathogen, and drug resistance of this organism continues to rise. Substantial efforts have been made to generate vaccines that provide long-lasting protection; however, these have fallen short. High-affinity antibodies could represent a useful treatment modality, taking advantage of effector functions to eliminate infecting bacteria. Many bacteria evade strong immune responses by encasing themselves in carbohydrate polymers. We have developed a means of generating high-affinity antibodies to small carbohydrate epitopes from bacteria. We describe here the design and synthesis of a disaccharide glycan from the capsular polysaccharide of S. aureus serotype 8, along with a selection/detection reagent for the characterization of antibody affinity for the targeted glycan. These materials were applied by conjugation of the disaccharide epitope to an immunogenic Qβ virus-like particle carrier protein with complete control of the position of attachment, generating a well-defined polyvalent immunogen. Without the use of additional adjuvants, this material generated a potent and long-lasting anti-glycan serum IgG response dominated by Th1 T cell help.
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2. Ferroptosis in neonatal and paediatric disease: From molecular mechanism to therapeutic target.
PMID:日期:2026-09-09Ferroptosis is an iron-dependent regulatory cell death mechanism mediated by lipid peroxidation. Increasing evidence suggests that this process is closely related to the etiology of a variety of paediatric diseases. This review systematically elaborates the core molecular mechanism of ferroptosis, and highlights that newborns exhibit organ‑specific susceptibility to ferroptosis, predominantly attributed to the convergence of high PUFA content in the developing brain and erythrocytes, immature antioxidant defences, and a propensity for free iron accumulation. Building on this, we further examine the role of ferroptosis in multiple childhood disorders, such as bronchopulmonary dysplasia, hypoxic-ischaemic encephalopathy, haemolytic hyperbilirubinemia, necrotizing enterocolitis, retinopathy of prematurity, and neonatal rotavirus‑associated biliary atresia. Furthermore, we synthesize existing evidence, which is largely preclinical, regarding therapeutic interventions that modulate ferroptosis, including iron chelators, selective inhibitors (e.g., ferrostatin-1), and activators of endogenous antioxidant pathways (e.g., Nrf2 inducers). We also discuss the multiple difficulties and challenges encountered by the current study in paediatric clinical trials, especially with respect to ferroptosis‑related issues. This review identifies a series of key barriers to clinical translational research in paediatric ferroptosis, based on a systematic review of the available evidence. In response to these obstacles, we propose a prioritized translational framework that focuses on juvenile animal models, age-stratified pharmacokinetics, and patient-derived organoids, to provide guidance for translating clinical practice to this vulnerable population.
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3. Exploring the impact of syndecans in prostate cancer: Stage-specific roles and therapeutic implications.
3. 探讨多配体蛋白聚糖在前列腺癌中的影响：分期特异性作用及治疗意义PMID:日期:2026-09-04Syndecans (SDCs) 1-4 are a family of transmembrane heparan sulfate proteoglycans (HSPGs) that regulate cell-cell communication, adhesion, extracellular matrix organization, and signaling pathways involved in tumor biology. In prostate cancer (PCa), accumulating evidence suggests that SDCs contribute to tumor progression, therapeutic resistance, and interactions within the tumor microenvironment. However, their specific, stage-dependent roles remain incompletely understood. This review provides an integrated synthesis of current experimental and clinical evidence on SDC1-SDC4 in PCa, complemented by exploratory analyses of publicly available transcriptomic, genomic, and proteomic datasets. In contrast, copy-number alteration (CNA) strata dichotomized by the mean for SDC1, SDC2, and SDC4 showed differences in progression-free interval. Specific CNA subclasses and relationships between CNA values and SDC mRNA or protein abundance could not be determined. Proteomic pseudotime analysis further suggested that SDC4 expression increases during PCa progression, supporting its potential involvement in advanced disease. We discuss the regulation and modulation of SDCs by androgen deprivation therapy (ADT), enzymatic shedding, integrin-mediated signaling, extracellular matrix interactions, lipid signaling pathways, and microRNA networks. In particular, SDC1-microRNA interactions may influence PCa cell proliferation, cellular senescence, epithelial-mesenchymal transition (EMT), and intracellular signaling pathways. Overall, this review highlights SDCs as context-dependent regulators of PCa biology with potential relevance as biomarkers or therapeutic targets. However, clinical translation will require independent validation, standardized assays, compartment-resolved analyses, and mechanistic confirmation.
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4. Bacterial LPS-induced inflammation reduces aquaglyceroporin-mediated glycerol permeability in TM3 mouse leydig cells and is associated with impaired mitochondrial respiration.
PMID:日期:2026-09-03Inflammation accompanies a wide range of pathological conditions and negatively impacts the male reproductive function by interfering with steroidogenesis and spermatogenesis. Steroidogenesis is sustained by Leydig cells (LCs), but it can be impaired by local or systemic inflammatory events known to alter the expression and function of aquaporins (AQPs). In addition, glycerol acts as an osmolyte and a metabolic substrate that supports cellular homeostasis and contributes to the proper function of testicular cells. To investigate the effects of inflammation on aquaglyceroporins (AQGPs) and glycerol transport, Mus musculus LCs (TM3) were exposed to bacterial lipopolysaccharide (LPS) for 24 h to induce an inflammatory-like state; this promoted a decrease in glycerol permeability, assessed by stopped-flow light scattering, and increased expression of the Aqp9 transcript. Furthermore, inflammatory stimulation was associated with impaired mitochondrial respiration activity, reflected by decreased oxygen consumption rates linked to ATP production (OCR), as well as reduced expression of the steroidogenic genes Star and Cyp17a1 and lower testosterone production. Collectively, these findings demonstrate that inflammation is associated with alterations in Aqp9 expression, glycerol permeability, mitochondrial respiratory parameters, and steroidogenic activity in TM3 mLCs. Though the mechanisms linking glycerol homeostasis, cellular energy metabolism, and hormone production under inflammatory conditions warrant further investigation, this work provides first-time evidence of a correlation between inflammation-induced metabolic and hormonal disruptions and impairment of glycerol transport in TM3 LCs.
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5. Corrigendum to "Immunogenicity of mRNA encoded MUC1 glycopeptides toward CAR-T cells" [Eur. J. Cell Biol. 105 (2026) 151543].
5. 关于“mRNA编码的MUC1糖肽对CAR-T细胞的免疫原性”的勘误 [Eur. J. Cell Biol. 105 (2026) 151543]PMID:日期:2026-09-01该文献暂无摘要。
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6. GOLPH3 depletion in glioblastoma cells promotes anti-tumor effects and neuronal differentiation by affecting mTOR signaling.
PMID:日期:2026-09-01Glioblastoma is the most aggressive primary brain tumor in adults. Resistance of glioblastoma to the standard chemotherapy agent temozolomide (TMZ) correlates with the expression of the DNA repair enzyme O6-Methylguanine-DNA methyltransferase (MGMT). Additionally, tumor initiation and recurrence are associated with a subpopulation of glioblastoma stem cells (GSCs) which exhibit self-renewal properties, multipotency, and resistance to both chemotherapy and radiotherapy. To identify novel molecular biomarkers and therapeutic targets, we investigated the possible role of the oncoprotein Golgi phosphoprotein 3 (GOLPH3) in glioblastoma. GOLPH3 is overexpressed in many solid tumors and confers resistance to DNA-damaging chemotherapeutic agents. Its overexpression is also associated with poor prognosis in a variety of cancers, including glioblastoma. Here, we show that GOLPH3 knockdown in U87MG glioblastoma cells inhibits cell proliferation, promotes senescence and induces striking cellular and molecular changes toward a neuron-like phenotype. We analyzed the constitutive expression of GOLPH3, MGMT and mechanistic target of rapamycin (mTOR) signaling proteins in U87MG cells and in three GSCs representative of the three glioblastoma molecular subtypes. Our results suggest that these glioblastoma cell models may exhibit distinct responses to mTOR inhibition and TMZ. Finally, we show that GOLPH3 depletion reduces the activity of both mTOR complex 1 and 2 leading to decreased phosphorylation of their respective downstream targets S6K and Akt in both U87MG cells and the BT379 GSCs subtype. Our findings identify a potential therapeutic vulnerability that can be exploited to develop patient-tailored treatments in glioblastoma.
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7. Spatiotemporal dynamics of epididymal epithelial cells uncover a novel KRT5⁺ATP6V1A⁺ subpopulation of basal cell in postnatal mouse development.
PMID:日期:2026-09-01Epididymal epithelial cells are critical for sperm maturation. Although previous studies have determined the development of epididymal epithelial cells in rat epididymis, the postnatal developmental trajectories of distinct epithelial cell types in the mouse epididymis remain elusive. Here, we examined the developmental timeline of mouse epididymal epithelium differed from that of the rat by confocal immunostaining and single-cell RNA sequencing (scRNA-seq). In mice, principal and basal cells appeared as early as postnatal day 7 (PD7) across all segments, labeled by AQP9 and KRT5, in contrast to the later emergence in rats (e.g., basal cells at PD14 in rat cauda). ATP6V1A-positive clear cells were detected at PD28 in caput, corpus, and cauda but not in the initial segment, while narrow cells were observed in all segments beginning at PD14. These contrasted with the rat, in which clear cells appeared at PD14. Notably, scRNA-seq and immunostaining identified a previously unrecognized KRT5⁺/ATP6V1A⁺ narrow-like basal cell subpopulation, enriched in lysosomes and mainly localized to the caput and corpus. These findings revealed an earlier epithelial maturation in mice compared to rats, underscoring the importance of choosing animal models. The newly identified basal subpopulation may contribute to luminal acidification and homeostasis, offering new insights into epididymal physiology and reproductive biology.
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8. Mutations in nucleoporins and their roles in human diseases: Integrating evidence on specific NUP functions.
PMID:日期:2026-09-01Nuclear pore complexes (NPCs), massive assemblies of approximately 30 distinct nucleoporins (NUPs), serve as the major gateways for nucleocytoplasmic transport. Recent research highlights that NUP aberrations-ranging from gene fusions and mutations to pathological protein accumulation-are increasingly implicated in the pathogenesis of a broad spectrum of human diseases. The underlying pathogenic mechanisms are highly multifactorial, encompassing the structural collapse of the NPC, transport network paralysis, epigenetic hijacking via liquid-liquid phase separation, and off-pore transcriptional dysregulation. This review synthesizes the multifaceted molecular etiology of NUP-associated pathologies. A deeper understanding of these diverse functions will shed light on the broader biological roles of NUPs and guide future research into targeted and personalized therapeutic strategies for NUP-associated disorders.
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9. Potential of a bacterial immunomodulatory enzyme to restore health in a Th1 cytokine cocktail induced skin psoriasis-like model.
PMID:日期:2026-09-01Psoriasis is a chronic inflammatory disorder driven by immune dysregulation. A common characteristic is hyperproliferation and aberrant differentiation of keratinocytes. Th1-type cytokines, containing TNFα, IL-1α and IL-6, play a role in various cellular processes such as the activation of dendritic cells, antigen processing and presentation, cell adhesion and migration, as well as cytokine and chemokine production. They are believed to be key contributors to the pathogenesis of psoriasis. In this work, healthy human epidermis equivalents (HEEs) were developed using neonatal human epidermal keratinocytes. Psoriatic-like HEEs were created by stimulating healthy HEEs with a Th1 cytokine cocktail containing TNFα, IL-1α and IL-6. Streptococcal C5a peptidase (ScpA), a powerful anaphylatoxin, was investigated as a potential anti-inflammatory therapeutic in this model. Although ScpA does not cleave any of these cytokines directly, it has been reported to cleave complement factors, C5a and C3, and the inflammatory cytokine, interferon gamma - all markers elevated in psoriasis. Histological and barrier function studies revealed that the cellular barrier was compromised under psoriatic-like conditions induced by the Th1 cytokine cocktail, while treatment with ScpA and retinoic acid restored the barrier function. Immunofluorescence and gene expression analyses further demonstrated that treatment with ScpA promoted the recovery of psoriatic-like HEEs towards a healthy HEE phenotype. Taken together, the results indicated that ScpA provided greater restoration of health in an in vitro Th1 cytokine cocktail-induced psoriasis-like model than a standard psoriasis drug.
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10. Epigenetic regulation of non-apoptotic regulated cell death.
PMID:日期:2026-09-01For decades, apoptosis has reigned supreme in cell death therapeutics, yet its clinical limitations in resistant cancers and degenerative diseases have unveiled the critical role of non-apoptotic regulated cell death (RCD) pathways, including ferroptosis, necroptosis, pyroptosis, and parthanatos. This review examines chromatin as a key regulatory layer influencing these pathways through dynamic histone modifications, DNA methylation, non-coding RNAs, and 3D genome architecture. We dissect how chromatin landscapes integrate metabolic, oxidative, and inflammatory signals in a cell-type- and lineage-dependent manner to steer cell fate, thereby enabling context-specific RCD activation or suppression. Emerging evidence suggests that epigenetic dysregulation can silence tumor-suppressive cell-death regulators such as GSDME and RIPK3 in some cancers and may contribute to neuronal susceptibility to parthanatos in specific neurodegenerative models. Therapeutically, the reversibility of epigenetic marks makes HDAC/DNMT inhibitors, BET-targeting agents, and CRISPR/dCas9-based editing attractive candidates for re-sensitizing selected preclinical models to RCD inducers; however, their clinical value will depend on improving tissue selectivity, minimizing toxicity, and demonstrating durable efficacy in heterogeneous patient tumors. Nanotechnology may improve delivery, but it does not fully overcome systemic exposure or targeting barriers. Emerging frontiers (single-cell epigenomics, phase-separated biomolecular condensates, and mitochondrial-nuclear crosstalk) may help identify candidate biomarkers and vulnerabilities, but these remain incompletely validated. By shifting from a genetic to a chromatin-centric paradigm and explicitly accounting for cell-type-specific chromatin states, this review highlights a promising framework for overcoming cell-death resistance, while recognizing that most pathway links, biomarkers, and delivery strategies still require robust validation in vivo and across patient cohorts before broad clinical translation.