Journal of Extracellular Vesicles细胞外囊泡杂志
Journal of Extracellular Vesicles(英文缩写 J EXTRACELL VESICLES),ISSN 2001-3078,eISSN 2001-3078,中文译名:细胞外囊泡杂志 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：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
Journal of Extracellular Vesicles 最新收录文献
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1. Bacterial Cytochrome C Orchestrates Larval Metamorphosis Through Bioelectrical Control of Extracellular Vesicles Biogenesis.
1. 细菌细胞色素C通过生物电控制细胞外囊泡生物发生来协调幼虫变态PMID:日期:2026-09-30Beyond the well-established roles in biomedical processes, extracellular vesicles (EVs) from Gram-negative bacteria are now identified as potent inducers of larval metamorphosis in marine invertebrates, a critical process for sustaining the health and function of global marine ecosystems. However, the specific inductive molecules within EVs remain largely unknown. Our findings reveal that cytochrome c (CytC), a previously unrecognized chemical signal packaged within EVs, induces larval metamorphosis. CytC maturation is essential for this process, as it enhances the efficiency of electron transfer, thereby supplying the energy required for EV biogenesis and loading with CytC cargo. Molecular docking analysis suggests that bacterial CytC induces the metamorphosis of mussels by binding to Toll-like receptor 4 (TLR4). Notably, a marked rise in CytC gene abundance was observed in the associated bacterial community during larval metamorphosis, which may indicate a programmed enhancement of electrogenic activity within the biofilm microenvironment to support larval developmental transition. Overall, a new paradigm for interkingdom signaling is proposed in this study, wherein CytC serves as a bioelectrical driver of EV biogenesis and a potentially broadly acting inductive signal within EVs for larval metamorphosis in invertebrates.
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2. Enrichment and Proteomic Profiling of Stromal-Associated Extracellular Vesicle Subpopulations From Arthritic Synovial Fluid by Size-Exclusion Chromatography Coupled to CD90-Directed Immunocapture.
2. 通过体积排阻色谱结合CD90定向免疫捕获技术对关节炎滑液中基质相关细胞外囊泡亚群进行富集及蛋白质组学分析PMID:日期:2026-09-30Extracellular vesicles (EVs) are emerging as key mediators of disease-associated intercellular communication and as promising biomarker sources across many disease conditions, including joint disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA). Molecular profiling of synovial tissue has uncovered disease-driving cellular states, but tissue biopsies are invasive and not routinely available. EVs in synovial fluid may offer a minimally invasive and complementary window into joint pathobiology. However, the molecular complexity of synovial fluid and the heterogeneity of EV populations have hindered the analysis of defined disease-relevant EV subsets. To address this challenge, we developed a refined size-exclusion chromatography-ultrafiltration (SEC-UF) workflow coupled to magnetic bead-based immunocapture for targeted enrichment of cell type-associated EV subpopulations from arthritic synovial fluid. As proof-of-concept, we targeted a stromal-associated EV population using CD90/THY1, a surface marker expressed by discrete synovial fibroblasts subsets implicated in arthritis pathobiology. In vitro validation using synovial fibroblast-derived EVs confirmed surface-accessible CD90 and demonstrated selective immunocapture of defined EV subpopulations. Application to patient-derived synovial fluid showed that SEC-UF pre-enrichment improves the robustness of CD90 EV recovery from this complex biofluid. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) profiling established broad EV-associated proteome coverage in synovial fluid (SF)-EV preparations and identified multiple proteins reflecting the inflamed arthritic synovial environment. Fraction-resolved proteomics enabled comparison of the CD90-immunocaptured SF-EV subset with the non-captured CD90/CD90 SF-EV pool. Differential proteomics and surfaceome-informed cell-of-origin analysis supported enrichment of stromal-associated surface markers in the CD90 fraction, whereas the non-captured SF-EV pool retained broader immune-associated and residual stromal EV inputs. Together, this fit-for-purpose workflow provides a strategy to resolve EV heterogeneity patient synovial fluid and supports future biomarker-oriented studies of defined subpopulations in arthritic diseases.
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3. Dual-Targeted M1 Macrophage Extracellular Vesicles Reprogram the Tumor Microenvironment and Enhance Natural Killer Cell Immunotherapy in Breast Cancer.
3. 双靶向M1型巨噬细胞细胞外囊泡重编程肿瘤微环境并增强乳腺癌自然杀伤细胞免疫治疗PMID:日期:2026-09-30Breast cancer is the most commonly diagnosed cancer worldwide and a leading cause of cancer-related mortality in women. Despite therapeutic advances, treating advanced or recurrent cases is substantially hampered by drug resistance and the immunosuppressive tumor microenvironment (TME). Here, we report a breakthrough immunotherapeutic strategy using dual-targeted extracellular vesicles from pro-inflammatory M1 macrophages, hyaluronic acid (HA), and cyclic RGD (M1EV_HA/cRGD), which function as molecular bridges to physically link natural killer (NK) cells with cancer cells. Our platform simultaneously reprograms the hostile TME while activating potent antitumor immunity. HA is incorporated to engage CD44 receptors on NK cells and cRGD peptides to bind tumor-overexpressing integrins, establishing precision dual-targeting. M1EV_HA/cRGD could physically tether NK cells directly to tumors, and deliver inflammatory cytokines and miRNAs that transform the immunosuppressive TME into a pro-inflammatory battlefield, substantially amplifying immune activation. In vitro and in vivo studies demonstrate that M1EV_HA/cRGD significantly enhances NK cell clustering at tumor sites, activation status, and cytotoxic killing of breast cancer cells. Unlike single-targeted approaches, this dual-targeting mechanism achieves simultaneous TME reprogramming and enhanced immune-tumor engagement. M1EV_HA/cRGD is a paradigm shift in solid tumor immunotherapy that directly addresses breast cancer treatment failure, can overcome therapeutic resistance, and substantially improve patient survival outcomes.
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4. Extracellular Vesicle-Bound Bacterial Toxin Pneumolysin Triggers Membrane Engagement and Damage Beyond Canonical Pore Formation.
PMID:日期:2026-09-30Pneumolysin (PLY) is a cholesterol-dependent pore-forming toxin and a key virulence factor of Streptococcus pneumoniae, the leading cause of pneumonia worldwide in children aged below 5 years. At sublytic toxin doses, host cells shed PLY-laden extracellular vesicles (EVs) during the membrane repair response. However, it remains unclear how these toxin-bearing EVs engage and damage target cell membranes. Here, we combine molecular dynamics simulations, liposome fusion assays and cell-based experiments to elucidate the membrane interaction potential of vesicle-bound PLY. Simulations indicate that EV-embedded PLY uses an exposed helix to bind target cell membranes, inducing pronounced curvature, bilayer thinning and water influx. Liposome fusion assays by 3D confocal imaging and Cryo-EM analysis demonstrate that both PLY and membrane cholesterol promote vesicle-membrane interactions. Characterisation of vesicle subpopulations released from PLY-challenged monocytes by western blotting and immunogold electron microscopy demonstrated that plasma membrane-derived microvesicles are preferentially enriched in membrane-bound PLY compared to small extracellular vesicles. Consistent with these findings, MVs purified from wild-type PLY-challenged monocytes, fuse with human peripheral blood mononuclear cells, delivering toxin and causing membrane damage, which was significantly lower with the toxoid mutant, PLYW433F. Among PBMCs, CD4 T cells showed higher PLY positivity upon MV co-incubation and higher cell death compared to monocytes at same dose. Together, our results reveal a noncanonical mode of toxin dissemination, in which vesicle-bound pneumolysin fuses and destabilises target cell membranes, representing an alternative pathway for EV-mediated toxin activity and a potential target for therapeutic intervention.
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5. Conserved and Tissue-Specific RNA and Protein Cargos of Small Extracellular Vesicles From 120 Tissue Sites Across 34 Organs in a Single Pig.
5. 单一猪体内34个器官120个组织部位小细胞外囊泡的保守性和组织特异性RNA及蛋白质货物PMID:日期:2026-09-29Small extracellular vesicles (sEVs) carry diverse cargo essential for intercellular communication, but their organism-wide characterization across all tissues is still limited. Here, we present a multi-omics sEV atlas covering the whole-body of 120 tissue sites, four body fluids and nine gastrointestinal contents from the same pig. We identified 7995 proteins, 337 miRNAs as well as 105,409 transcripts (93,409 full-length) in sEVs by mass spectrometry, next- and third-generation RNA sequencing. Among these, a conserved cargo set of 252 proteins, 18 miRNAs and 1227 transcripts was defined, including RNA-binding proteins (ANXA2, ALIX and MVP), mitochondrial proteins (ATP5F1A, COX6C and VDACs), the let-7 miRNA family and ferritin genes (FTH1/FTL). Notably, sEV biogenesis-associated ACTG1, CFL1 and ANXA2 were detected in all samples, suggesting their potential as novel sEV protein markers. In contrast, 2638 proteins, 152 miRNAs and 1000 transcripts showed organ-specific expression patterns, which are likely to underpin organ-specific biological processes. Moreover, by using this multi-omic dataset and additional RIP assays, we found that HNRNPU participates in the sorting of hypoxia-responsive EPAS1 into sEVs. This comprehensive sEV atlas establishes a foundation for future studies in sEV cell biology.
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6. Shear Stress-Stimulated Trafficking of Endothelial Piezo1 to Splenic Capsule Boosts Spleen Contraction and Exercise Endurance.
6. 剪切应力刺激内皮Piezo1向脾囊运输，增强脾收缩和运动耐力PMID:日期:2026-09-28Haemodynamic shear stress, sensed by vascular endothelial cells (ECs), is crucial for the functional integrity of ECs and the systemic benefits of exercise. Here, we observed that shear stress triggers the release of medium/large extracellular vesicles (m/lEVs), from ECs via activation of the mechanosensitive ion channel Piezo1. Endothelial Piezo1 activation induces Piezo1 translocation to the cell periphery, facilitating its trafficking from the vascular ECs to the smooth muscle cells in the splenic capsule. Within the splenic capsule, the translocated Piezo1 acts as a downstream effector of α1-adrenergic receptor, boosting exercise-induced spleen contraction and enhancing exercise endurance. Genetic or pharmacological inhibition of Piezo1 trafficking from ECs impaired spleen contraction during exercise and reduced exercise endurance in mice. Additionally, exercise-induced m/lEV release contributes to safeguard endothelial function through modulating intracellular Piezo1 homeostasis. Furthermore, positive correlations between exercise-induced increases in circulating Piezo1-enriched m/lEVs and the degree of spleen contraction were also observed in human volunteers. These findings unveil a vasculo-splenic axis during exercise, in which EC-derived m/lEVs shuttle Piezo1 to maintain endothelial function and exercise endurance, highlighting a novel role of Piezo1 in inter-organ communication.
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7. Helicobacter pylori Outer Membrane Vesicles Engage TLR2 Through NapA to Promote Epithelial Association and Inflammatory Signalling.
7. 幽门螺杆菌外膜囊泡通过NapA参与TLR2以促进上皮黏附与炎症信号传导PMID:日期:2026-09-28Helicobacter pylori infection is characterized by chronic gastric inflammation driven by persistent activation of innate immune signalling pathways. Outer membrane vesicles (OMVs) released by H. pylori are important mediators of host-pathogen interactions. Although several mechanisms of OMV internalization have been described, how specific OMV-associated bacterial factors engage host innate immune receptors and couple vesicle association to inflammatory signalling remains poorly understood. Here, we investigated the contribution of OMV-associated virulence factors and Toll-like receptor 2 (TLR2) heterodimers to OMV-host cell interactions in gastric epithelial cells. Using engineered AGS and GES-1 reporter cells expressing TLR2/1 or TLR2/6, together with genetically defined OMVs, we found that H. pylori OMVs preferentially associated with TLR2-expressing cells and induced robust NF-κB activation. Comparative analysis of OMVs from wild-type and isogenic mutant strains identified Neutrophil-Activating Protein A (NapA) as a major determinant of TLR2-dependent OMV association and inflammatory signalling, whereas urease had a more limited contribution. Disruption of NapA or neutralization of TLR2 markedly reduced OMV association with gastric epithelial cells. Purified H. pylori lipopolysaccharide elicited a comparatively weak and TLR2/6-biased response, indicating that it does not account for the robust TLR2-dependent signalling induced by intact OMVs. Furthermore, OMV-associated NapA exhibited greater pro-inflammatory activity than soluble recombinant NapA, supporting a role for the vesicular context in enhancing TLR2-dependent signalling. Pharmacological inhibition with sulforaphane significantly attenuated OMV-induced TLR2/NF-κB activation. Collectively, these findings identify a previously unrecognized role for OMV-associated NapA in linking TLR2-dependent vesicle association with gastric epithelial cells to inflammatory signalling and support a model in which vesicular presentation.
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8. Extracellular Vesicle-Encapsulated Small RNAs From Clostridium Butyricum Modulate Host Intestinal Lipid Metabolism.
PMID:日期:2026-09-28The gut microbiota plays a critical role in regulating intestinal lipid metabolism, yet the mechanisms governing microbiota-host interactions during lipid uptake remain unclear. Here, we examined the relationship between fat digestibility and gut microbial composition, and found that piglets with higher apparent crude fat digestibility exhibited enhanced lipid absorption and oxidation, accompanied by reduced abundance of Clostridium butyricum in the ileal mucosa. Furthermore, oral administration of C. butyricum suppressed intestinal lipid absorption and oxidation by inhibiting PPARα signaling. Mechanistically, extracellular vesicles (EVs) derived from C. butyricum can enter intestinal epithelial cells and mediate the anti-lipid absorption effects by delivering miRNA-like RNAs (milRNAs), particularly milRNA-3020179, which primarily targeted host genes including PPARα and Rxra. Supplementation with C. butyricum or its EVs prevented lipid accumulation and attenuated the development of metabolic abnormalities in high-fat diet-fed mice, whereas deletion of milRNA-3020179 in C. butyricum abolished its effects on lipid deposition in intestinal organoids. Collectively, these findings identify C. butyricum-derived EV milRNAs as candidate microbial regulators of host lipid metabolism through modulation of PPARα signaling, providing insights into microbiota-driven control of intestinal lipid homeostasis.
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9. Trophoblast Extracellular Vesicles Rewire Immunity: A Symptom-Relief Avenue for Recessive Dystrophic Epidermolysis Bullosa.
9. 滋养层细胞外囊泡重塑免疫：隐性营养不良型大疱性表皮松解症的缓解症状新途径PMID:日期:2026-09-24Redirecting immune responses toward tissue repair represents a promising strategy for treating inflammatory and degenerative diseases. Extracellular vesicles (EVs), derived from allogeneic stem cells, have shown potential for modulating proinflammatory immunity. Among these, placental-derived EVs (PEVs) are emerging as candidates for immune-mediated inflammatory disorders due to their role in establishing maternal immune tolerance. However, their applicability beyond pregnancy remains limited by key translational barriers, including the lack of a standardized and scalable source system and need to demonstrate immunomodulatory activity in non-pregnancy allogeneic contexts. In this study, we identify extravillous trophoblasts (EVTs), which play critical role in early placental development, as key source of immunoregulatory PEVs. To overcome donor variability, we employed the HIPEC cell model as established surrogate for primary EVTs and assessed the effects of their derived EVs (EVT-EVs) on circulating monocytes, pivotal mediators of inflammatory responses. High-dimensional molecular profiling revealed that EVT-EVs, similar to EVs derived from first-trimester primary human trophoblast, carry a distinctive anti-inflammatory signature, including a unique miRNA repertoire enriched in immunoregulatory pathways. Integrated proteomic and lipidomic analyses demonstrated that EVT-EVs induce coordinated functional reprograming of monocytes toward an immunomodulatory, inflammation-resolving phenotype. Notably, EVT-EVs also modulated the inflammatory bias of monocytes from patients with recessive dystrophic epidermolysis bullosa (RDEB), a genetic disorder characterized by chronic inflammation, thereby promoting restoration of immune balance. Collectively, these findings identify EVT-EVs as a scalable, off-the-shelf platform with high translational potential for the treatment of chronic inflammatory diseases.
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10. Oxylipins-Omics Combine With Single-Molecule Analysis Identifies 13(S)-HODE Positive Extracellular Vesicles as a Diagnostic Biomarker for AFP-Negative Hepatocellular Carcinoma.
PMID:日期:2026-09Efficient diagnostic biomarkers enable early detection of hepatocellular carcinoma (HCC), which improves survival. Circulating extracellular vesicles (EVs) in plasma, as a noninvasive diagnostic carrier, have caused widely concern. Here, a novel oxylipidomic profiling was used to analysis the HCC patients' tissue-derived EVs (TD-EVs) cargo and revealing differentially expressed oxylipins (vs. adjacent tissues, p<0.05), which undetected in bulk tissues. The hub oxylipins 13(S)-HODE discovered in TD-EVs was validated in plasma derived EVs (PD-EVs) by using single-molecule analysis platform, showing superior efficacy in AFP-negative HCC patients (AUC = 0.8474 vs. 0.7627 in AFP-positive). Clinically, machine learning integrating EV-derived 13(S)-HODE with routine clinical parameters of HCC patients was developed to optimize diagnostic classification. The machine learning model, LightGBM, achieved outstanding performance: AUC_mean = 0.962, Sensitivity = 0.933 (0.660-0.997), Specificity: 0.957(0.760-0.998), 95%CI: 0.958-1.000 in multi-group classification of HCC diagnostics, demonstrating the enhanced diagnostic efficiency of 13(S)-HODE positive EV subpopulation with other clinical data. This study firstly establishes EV-derived 13(S)-HODE as a concordantly biomarker across tissue and plasma sources. Furthermore, single-molecule analysis platform offers it a highly sensitive diagnostic performance for HCC, particularly valuable for AFP-negative HCC subgroup.