IF 10.7

MedComm Pub Date : 2025-09-14 DOI: 10.1002/mco2.70350

Rongli Xie, Guohui Xiao, Kaige Yang, Xiaofeng Wang, Cong Chen, Min Ding, Tong Zhou, Rajarshi Mukherjee, Robert Sutton, Erzhen Chen, Ying Chen, Wei Huang, Dan Xu, Jian Fei

{"title":"Single-Cell Transcriptomic Atlas of Peripheral Blood Reveals B-Cell-Driven Signature Predictive of Acute Pancreatitis Severity","authors":"Rongli Xie, Guohui Xiao, Kaige Yang, Xiaofeng Wang, Cong Chen, Min Ding, Tong Zhou, Rajarshi Mukherjee, Robert Sutton, Erzhen Chen, Ying Chen, Wei Huang, Dan Xu, Jian Fei","doi":"10.1002/mco2.70350","DOIUrl":"https://doi.org/10.1002/mco2.70350","url":null,"abstract":"Effective early prediction of acute pancreatitis (AP) severity remains an unmet clinical need due to limited molecular characterization of systemic immune responses. We performed integrated single-cell RNA sequencing with T- and B-cell receptor profiling on peripheral blood mononuclear cells from AP patients (n = 7) at days 1, 3, and 7 after admission. Immune landscape analysis revealed marked inter-patient heterogeneity, with a distinct expansion of MZB1-expressing plasma cells that were strongly associated with complicated AP and recovery. Functional validation in an independent cohort (n = 14) confirmed disease-associated plasma cell markers, alongside altered serum immunoglobulin and cytokine profiles (n = 32). From these findings, we established a nine-gene B-cell-derived transcriptomic signature (S100A8, DUSP1, JUN, HBA2, FOS, CYBA, JUNB, S100A9, and WDR83OS) predictive of AP severity. This model demonstrated high discriminative performance in internal validation (n = 114; AUROC > 0.95, superior to standard clinical scoring systems), and sustained accuracy in external validation cohorts of AP (n = 87) and AP combined with non-AP sepsis (n = 174) for predicting persistent organ failure. Our study identifies a mechanistic and predictive role for MZB1⁺ plasma cells in AP pathogenesis, offering a novel immune-based stratification strategy with potential for precision clinical management.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70350","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus-Like Disease by Inhibiting the IL-38-Ferroptosis Axis 嗜丁酸蛋白3A1通过抑制IL-38-Ferroptosis轴参与炎症并诱导狼疮样疾病

IF 10.7

MedComm Pub Date : 2025-09-14 DOI: 10.1002/mco2.70356

Wang-Dong Xu, Da-Cheng Wang, Yang-Yang Tang, Qi Huang, Lu Fu, You-Yue Chen, Lu-Qi Yang, Si-Yu Feng, Lin-Chong Su, An-Fang Huang

{"title":"Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus-Like Disease by Inhibiting the IL-38-Ferroptosis Axis","authors":"Wang-Dong Xu, Da-Cheng Wang, Yang-Yang Tang, Qi Huang, Lu Fu, You-Yue Chen, Lu-Qi Yang, Si-Yu Feng, Lin-Chong Su, An-Fang Huang","doi":"10.1002/mco2.70356","DOIUrl":"https://doi.org/10.1002/mco2.70356","url":null,"abstract":"Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown origin. Recent evidence has linked butyrophilin 3A1 (BTN3A1) to immune dysregulation. This study was to elucidate the relationship of BTN3A1 in SLE. Expression of BTN3A1 in plasma and peripheral blood mononuclear cells from SLE patients and healthy controls explored the association between BTN3A1 and SLE. We found that BTN3A1 mRNA, plasma levels, and expression in CD4+ T cells were significantly elevated in SLE patients. In BTN3A1 gene knock-in (BTN3A1KI) mice, inflammation and lupus-like manifestations occurred, including increased proportions of Th1, Th2, and Th17 cells, decreased Treg cells, elevated levels of inflammatory cytokines and anti-dsDNA antibodies, renal injury, and suppressed IL-38 serum levels. Intraperitoneal injection of IL-38 in pristane-treated BTN3A1KI mice notably alleviated these pathological changes. Mechanistic investigations revealed that CD4+ T cells and the ferroptosis pathway were closely associated with the effects mediated by the BTN3A1-IL-38 axis. In vitro experiments showed that IL-38 stimulation reduced proliferation, apoptosis, and decreased the expression of ferroptosis-related proteins, Fe2⁺, glutathione, and malondialdehyde in CD4+BTN3A1+/+ T and BTN3A1+/+ Jurkat T cells. Overall, BTN3A1 plays a crucial role in SLE pathogenesis by regulating CD4+ T cell function.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70356","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transforming Cancer Diagnostics: The Emergence of Liquid Biopsy and Epigenetic Markers 改变癌症诊断：液体活检和表观遗传标记的出现

IF 10.7

MedComm Pub Date : 2025-09-14 DOI: 10.1002/mco2.70388

Debalina Saha, Pritam Kanjilal, Mandeep Kaur, Soumya V. Menon, Ayash Ashraf, M. Ravi Kumar, Taha Alqahtani, Shikha Atteri, Daniel Ejim Uti, Bikram Dhara

{"title":"Transforming Cancer Diagnostics: The Emergence of Liquid Biopsy and Epigenetic Markers","authors":"Debalina Saha, Pritam Kanjilal, Mandeep Kaur, Soumya V. Menon, Ayash Ashraf, M. Ravi Kumar, Taha Alqahtani, Shikha Atteri, Daniel Ejim Uti, Bikram Dhara","doi":"10.1002/mco2.70388","DOIUrl":"https://doi.org/10.1002/mco2.70388","url":null,"abstract":"Liquid biopsy represents a transformative approach in oncology, enabling noninvasive disease detection and monitoring through epigenetic signals in circulating tumor DNA (ctDNA), nucleosomes, and noncoding RNAs. Tumor initiation is driven by epigenetic modifications, including DNA methylation, histone alterations, and dysregulated noncoding RNAs, which disrupt gene regulation, cell cycle control, DNA repair, and metastatic processes. This review systematically examines recent evidence on DNA methylation, histone marks (e.g., H3K27me3, H3K18ac), and noncoding RNAs (miRNAs, lncRNAs) as biomarkers for early cancer detection, prognosis, and therapeutic response. Particular focus is placed on aberrant DNA methylation (e.g., hypermethylation of CDKN2A, RASSF1A) and altered histone modifications (e.g., EZH2-mediated silencing) as indicators of tumor heterogeneity and evolution. Stable and specific in biofluids, noncoding RNAs such as oncogenic miR-21, tumor-suppressive miR-34a, and metastasis-associated MALAT1/HOTAIR further enhance clinical applicability. Recent detection methods, including bisulfite sequencing, ChIP-seq, and RNA-seq, have advanced biomarker profiling, though challenges remain in standardization and low-abundance detection. With over 12 active clinical studies validating their utility, integration of epigenetic markers with AI and multiomics holds promise for individualized, dynamically guided oncology care. Future innovations, such as chromatin accessibility analysis and cfDNA fragmentation profiling, may further refine diagnostic precision and therapeutic monitoring.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70388","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Natural Killer Cell-Mediated Antitumor Immunity: Molecular Mechanisms and Clinical Applications 自然杀伤细胞介导的抗肿瘤免疫：分子机制和临床应用

IF 10.7

MedComm Pub Date : 2025-09-14 DOI: 10.1002/mco2.70387

Nanzhi Luo, Cong Chen, Wenjing Zhou, Jianqi Hao, Song He, Yu Liu, Yin Ku, Linhua Huang, Chuanfen Zhang, Yueli Shu, Xiaoqing Wu, Yaojia Zhou, Jian Zhang

{"title":"Natural Killer Cell-Mediated Antitumor Immunity: Molecular Mechanisms and Clinical Applications","authors":"Nanzhi Luo, Cong Chen, Wenjing Zhou, Jianqi Hao, Song He, Yu Liu, Yin Ku, Linhua Huang, Chuanfen Zhang, Yueli Shu, Xiaoqing Wu, Yaojia Zhou, Jian Zhang","doi":"10.1002/mco2.70387","DOIUrl":"https://doi.org/10.1002/mco2.70387","url":null,"abstract":"Natural killer (NK) cells are pivotal effectors in innate antitumor immunity by mediating cytotoxicity, secreting cytokines, or expressing cell membrane receptors, which facilitate interactions with other immune cells. The cytotoxic activity and immune function of NK cells are governed by dynamic receptor–ligand interactions, cytokine networks, and metabolic–epigenetic crosstalk within the tumor microenvironment (TME). Recent years, NK cell-based therapies are emerging as a promising clinical approach for antitumor treatment, owing to their rapid response, unique recognition mechanisms, potent cytotoxic capabilities, and memory-like characteristics, along with their low risk of posttreatment adverse effects and cost effectiveness. However, immunosuppression and metabolic reprogramming driven by TME subvert NK cell surveillance, impairing its antitumor function. This review comprehensively details molecular mechanisms underpinning NK cell dysfunction, including dysregulated activating/inhibitory receptor signaling, metabolic reprogramming, and epigenetic silencing of effector genes. We further synthesize advances in clinical strategies to restore NK cytotoxicity including ex vivo expansion for adoptive transfer, chimeric antigen receptor-NK engineering, TME-remodeling agents, immune checkpoint blockade, cytokine-based therapies, and NK cell engagers targeting tumor antigens. By bridging mechanistic insights with translational applications, this work provides a framework for rationally designed NK cell-based immunotherapies to overcome resistance across solid and hematologic malignancies.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70387","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glycolysis-Histone Lactylation Crosstalk Drives TXNIP-NLRP3-Mediated PANoptosome Assembly and PANoptosis Activation Underlying Diabetic Retinopathy Pathogenesis 糖酵解-组蛋白乳酸化串音驱动txnap - nlrp3介导的泛光小体组装和泛光功能激活：糖尿病视网膜病变发病机制

IF 10.7

MedComm Pub Date : 2025-09-14 DOI: 10.1002/mco2.70351

Xiaoting Xi, Qianbo Chen, Jia Ma, Xuewei Wang, Yuxin Zhang, Qiuxia Xiong, Xiaolei Liu, Yuan Xia, Yan Li

{"title":"Glycolysis-Histone Lactylation Crosstalk Drives TXNIP-NLRP3-Mediated PANoptosome Assembly and PANoptosis Activation Underlying Diabetic Retinopathy Pathogenesis","authors":"Xiaoting Xi, Qianbo Chen, Jia Ma, Xuewei Wang, Yuxin Zhang, Qiuxia Xiong, Xiaolei Liu, Yuan Xia, Yan Li","doi":"10.1002/mco2.70351","DOIUrl":"https://doi.org/10.1002/mco2.70351","url":null,"abstract":"Diabetic retinopathy (DR), a major cause of vision loss in adults, involves aberrant metabolism and inflammation. This study investigated the interplay between glycolysis, histone lactylation, and PANoptosis in DR using human retinal pigment epithelial (RPE) cells under high glucose and diabetic mouse models. Results demonstrated a positive feedback loop where enhanced glycolysis increased histone lactylation, which in turn further promoted glycolysis. This cycle activated the expression of thioredoxin interacting protein (TXNIP) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3), leading to PANoptosome formation and triggering PANoptosis, a coordinated cell death pathway contributing to DR pathology. Crucially, experiments manipulating TXNIP expression (via RNAi or overexpression) confirmed its central role in linking histone lactylation to NLRP3 activation and PANoptosome assembly. Importantly, inhibiting glycolysis or downregulating TXNIP successfully reduced histone lactylation, suppressed PANoptosome formation, and alleviated PANoptosis. These findings establish that the glycolysis-histone lactylation axis, mediated by TXNIP/NLRP3 signaling, drives PANoptosis in RPE cells through PANoptosome formation, playing a critical role in DR development. Targeting this specific pathway presents a promising new therapeutic strategy for diabetic retinopathy.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70351","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Novel Genetic TDP-43 Pig Model Mimics Multiple Key ALS-Like Features 一种新的遗传TDP-43猪模型模拟了多个关键的als样特征

IF 10.7

MedComm Pub Date : 2025-09-14 DOI: 10.1002/mco2.70330

Chunhui Huang, Xiao Zheng, Jiaxi Wu, Jiawei Li, Yingqi Lin, Yizhi Chen, Caijuan Li, Xichen Song, Wei Wang, Zhaoming Liu, Jianhao Wu, Jiale Gao, Zhuchi Tu, Zaijun Zhang, Liangxue Lai, Shihua Li, Xiao-Jiang Li, Sen Yan

{"title":"A Novel Genetic TDP-43 Pig Model Mimics Multiple Key ALS-Like Features","authors":"Chunhui Huang, Xiao Zheng, Jiaxi Wu, Jiawei Li, Yingqi Lin, Yizhi Chen, Caijuan Li, Xichen Song, Wei Wang, Zhaoming Liu, Jianhao Wu, Jiale Gao, Zhuchi Tu, Zaijun Zhang, Liangxue Lai, Shihua Li, Xiao-Jiang Li, Sen Yan","doi":"10.1002/mco2.70330","DOIUrl":"https://doi.org/10.1002/mco2.70330","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that lacks ideal models to comprehensively recapitulate its pathological features. TDP-43 pathology, a hallmark of neurodegenerative diseases, plays a critical role in disease progression. Given the anatomical and physiological similarities between pig and human brains, large animal models offer a unique advantage in more accurately simulating patient-specific disease characteristics. In this study, we rapidly established a TDP-43-induced neurodegenerative disease model in pigs through ear vein injection of the TDP-43M337V virus. Disease progression was systematically evaluated using behavioral assessments and pathological analyses. This porcine model produced extremely severe motor dysfunction accompanied by significant muscle atrophy and fibrosis. Additionally, characteristic TDP-43 pathological phenotypes were observed, including degeneration of spinal motor neurons and proliferation of glial cells in both the brain and spinal cord. Notably, TDP-43M337V induction led to a significant upregulation of TMEM106B, SOD1, and APOE4 levels. This TDP-43 porcine model recapitulates multiple key features of ALS and serves as a valuable complement to existing animal models, providing a robust platform for investigating TDP-43-related pathogenic mechanisms of TDP-43 and developing effective therapeutics.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70330","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mitochondrial Diseases: Molecular Pathogenesis and Therapeutic Advances 线粒体疾病：分子发病机制和治疗进展

IF 10.7

MedComm Pub Date : 2025-09-12 DOI: 10.1002/mco2.70385

Jialun Mei, Peng Ding, Chuan Gao, Jian Zhou, Zhiwei Li, Changqing Zhang, Junjie Gao

{"title":"Mitochondrial Diseases: Molecular Pathogenesis and Therapeutic Advances","authors":"Jialun Mei, Peng Ding, Chuan Gao, Jian Zhou, Zhiwei Li, Changqing Zhang, Junjie Gao","doi":"10.1002/mco2.70385","DOIUrl":"https://doi.org/10.1002/mco2.70385","url":null,"abstract":"Mitochondrial diseases are a heterogeneous group of inherited disorders caused by pathogenic variants in mitochondrial DNA (mtDNA) or nuclear genes encoding mitochondrial proteins, culminating in defective oxidative phosphorylation and multisystem involvement. Key pathogenic mechanisms include heteroplasmy driven threshold effects, excess reactive oxygen species, disrupted mitochondrial dynamics and mitophagy, abnormal calcium signaling, and compromised mtDNA repair, which together cause tissue-specific energy failure in high demand organs. Recent advances have expanded the therapeutic landscape. Precision mitochondrial genome editing—using mitochondrial zinc finger nucleases, mitochondrial transcription activator-like effector nucleases, DddA-derived cytosine base editor, and other base editing tools—enables targeted correction or rebalancing of mutant genomes, while highlighting challenges of delivery and off-target effects. In parallel, metabolic modulators (e.g., coenzyme Q10, idebenone, EPI-743) aim to restore bioenergetics, and mitochondrial replacement technologies and transplantation are being explored. Despite these promising strategies, major challenges remain, including off-target effects, precise delivery, and ethical considerations. Addressing these issues through multidisciplinary research and clinical translation holds promise for transforming mitochondrial disease management and improving patient outcomes. By bridging the understanding of mitochondrial dysfunction with advanced therapeutic interventions, this review aims to shed light on effective solutions for managing these complex disorders.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70385","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145038074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plasmacytoid and CD141+ Myeloid Dendritic Cells Cooperation with CD8+ T Cells in Lymph Nodes is Associated with HIV Control 浆细胞样细胞和CD141+髓样树突状细胞与CD8+ T细胞在淋巴结中的合作与HIV控制有关

IF 10.7

MedComm Pub Date : 2025-09-12 DOI: 10.1002/mco2.70354

Joana Vitallé, Sara Bachiller, Beatriz Dominguez-Molina, Eirini Moysi, Sara Ferrando-Martínez, María Inés Camacho-Sojo, Isabel Gallego, Alberto Pérez-Gómez, María Reyes Jiménez-Leon, Carmen Gasca-Capote, Francisco José Ostos, Mohammed Rafii-El-Idrissi Benhnia, Laura E. Via, Antonio Mochón, Luis Fernando López-Cortes, Constantinos Petrovas, Richard A. Koup, Ezequiel Ruiz-Mateos

{"title":"Plasmacytoid and CD141+ Myeloid Dendritic Cells Cooperation with CD8+ T Cells in Lymph Nodes is Associated with HIV Control","authors":"Joana Vitallé, Sara Bachiller, Beatriz Dominguez-Molina, Eirini Moysi, Sara Ferrando-Martínez, María Inés Camacho-Sojo, Isabel Gallego, Alberto Pérez-Gómez, María Reyes Jiménez-Leon, Carmen Gasca-Capote, Francisco José Ostos, Mohammed Rafii-El-Idrissi Benhnia, Laura E. Via, Antonio Mochón, Luis Fernando López-Cortes, Constantinos Petrovas, Richard A. Koup, Ezequiel Ruiz-Mateos","doi":"10.1002/mco2.70354","DOIUrl":"https://doi.org/10.1002/mco2.70354","url":null,"abstract":"Dendritic cells (DC) are known to modulate antiviral immune responses; however, the knowledge about the role of different DC subsets in antiviral T cell priming in human tissues remains uncompleted. In the context of HIV infection, we determined the phenotype and location of plasmacytoid and CD141+ myeloid DCs (pDCs and mDCs) in lymph nodes of people living with HIV (PLWH). We found an interaction between pDCs and CD141+ mDCs with CD8+ T cells, being associated with participants’ viral levels in blood and tissue. Moreover, we demonstrated a higher and more polyfunctional superantigen- and HIV-specific CD8+ T cell response after the coculture with Toll-like receptor (TLR)-primed pDCs and CD141+ mDCs. Last, we showed the potential of programmed cell death-1 (PD-1) blocking using pembrolizumab to further increase antigen-specific CD8+ T cell response along with TLR agonists. Therefore, these results showed a cooperation between pDCs, CD141+ mDCs and CD8+ T cells in lymph nodes of PLWH, which is associated with higher HIV control, highlighting the importance of DC subsets crosstalk to achieve a more potent anti-HIV response and support the use of DC-based immunotherapies for HIV control.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70354","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145038075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exosome-Based Therapeutics: A Natural Solution to Overcoming the Blood–Brain Barrier in Neurodegenerative Diseases 基于外泌体的治疗：克服神经退行性疾病血脑屏障的自然解决方案

IF 10.7

MedComm Pub Date : 2025-09-12 DOI: 10.1002/mco2.70386

Min Sun, Feng Qin, Qian Bu, Yue Zhao, Xiaofeng Yang, Dingwen Zhang, Xiaobo Cen

{"title":"Exosome-Based Therapeutics: A Natural Solution to Overcoming the Blood–Brain Barrier in Neurodegenerative Diseases","authors":"Min Sun, Feng Qin, Qian Bu, Yue Zhao, Xiaofeng Yang, Dingwen Zhang, Xiaobo Cen","doi":"10.1002/mco2.70386","DOIUrl":"https://doi.org/10.1002/mco2.70386","url":null,"abstract":"Neurodegenerative diseases present significant therapeutic challenges, primarily due to the restrictive nature of the blood–brain barrier (BBB), which limits drug delivery to the brain. While the BBB is crucial for protecting the brain from harmful substances, it also hinders the effectiveness of treatments for neurodegenerative diseases. Consequently, there is an urgent need for innovative drug delivery systems capable of bypassing the BBB to improve therapeutic outcomes. Exosomes, as endogenous nanoscale carriers, offer substantial promise for brain-targeted drug delivery. Their unique characteristics, including the ability to cross biological barriers, high biocompatibility, intrinsic targeting capacity, natural intracellular transport mechanisms, and robust stability, render them highly promising candidates for drug delivery in the treatment of neurodegenerative disorders. This review delves into various engineering strategies for exosome-mediated targeted drug delivery and provides an in-depth analysis of the structural and functional properties of the BBB under normal and pathological conditions. We emphasize the potential of exosomes as drug delivery vehicles for the central nervous system, particularly in addressing neurodegenerative disorders. Furthermore, we address the key obstacles to the clinical application of exosome-based therapies and propose future research directions aimed at optimizing these methods to develop more effective treatment strategies.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70386","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145038073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhanced Angiogenic Potential of Electrically Stimulated Human Adipose-Derived Mesenchymal Stem Cells (MSCs) for Ischemic Tissue Regeneration 电刺激人类脂肪源性间充质干细胞（MSCs）对缺血组织再生的血管生成潜力增强

IF 10.7

MedComm Pub Date : 2025-09-09 DOI: 10.1002/mco2.70352

Jongdarm Yi, Seungjun Lee, Chiseon Ryu, Gaeun Kim, Junghyun Kim, Jae Young Lee

{"title":"Enhanced Angiogenic Potential of Electrically Stimulated Human Adipose-Derived Mesenchymal Stem Cells (MSCs) for Ischemic Tissue Regeneration","authors":"Jongdarm Yi, Seungjun Lee, Chiseon Ryu, Gaeun Kim, Junghyun Kim, Jae Young Lee","doi":"10.1002/mco2.70352","DOIUrl":"https://doi.org/10.1002/mco2.70352","url":null,"abstract":"Effective treatment of ischemic disease requires the reconstruction of blood vessels through the delivery of angiogenic factors, such as chemicals, proteins, and cells. In particular, substantial efforts have focused on enhancing the therapeutic potential of mesenchymal stem cells (MSCs) for treating ischemic diseases. In this study, we investigated the use of electrical stimulation (ES) to potentiate the proangiogenic properties of human adipose-derived MSCs. Electrically potentiated MSCs (epMSCs) were generated by applying optimized ES parameters (0.3 V, 100 Hz). EpMSCs exhibited significantly enhanced angiogenic potential, including upregulated expression of proangiogenic factors (e.g., vascular endothelial growth factor [VEGF]-A and hepatocyte growth factor) and improved endothelial cell migration and tube formation in vitro. Transcriptomic and proteomic analyses revealed activation of key angiogenic pathways, particularly VEGFA–VEGFR2 signaling, which plays a critical role in enhancing the functionality of epMSCs. In vivo studies using a murine hindlimb ischemia model demonstrated that epMSCs enhanced blood flow recovery, induced angiogenesis, and reduced muscle atrophy more effectively than unstimulated MSCs. Overall, these findings suggest that electrical potentiation of MSCs is a promising strategy for effectively enhancing their angiogenic capabilities for treating ischemic diseases.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70352","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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