IF 10.7

MedComm Pub Date : 2025-06-11 DOI: 10.1002/mco2.70240

Wei Wang, Manfei Si, Xinyu Qi, Hongxia Hu, Xiaole Sun, Juyan Liang, Jianghua Zhou, Xianmin Bi, Wei Zhao, Yuanyuan Wang, Liying Yan, Rong Li, Wei Chen, Jie Qiao

{"title":"The Clinical and Metabolic Profiles in Menstrual Changes Among Reproductive-Aged Women Post-COVID-19","authors":"Wei Wang, Manfei Si, Xinyu Qi, Hongxia Hu, Xiaole Sun, Juyan Liang, Jianghua Zhou, Xianmin Bi, Wei Zhao, Yuanyuan Wang, Liying Yan, Rong Li, Wei Chen, Jie Qiao","doi":"10.1002/mco2.70240","DOIUrl":"https://doi.org/10.1002/mco2.70240","url":null,"abstract":"Menstruation is a key indicator of female reproductive health, yet clinical features and underlying mechanisms associated with menstrual changes following the coronavirus disease 2019 (COVID-19) infection remain unclear. Here, we recruited 253 participants through questionnaires, and 73 individuals underwent metabolomic analysis of blood serum. Over 60% reported menstrual changes, primarily experiencing longer cycle and lighter bleeding, which were significantly associated with age, general medical conditions, perceived stress, anxiety scores, and depression scores, as well as COVID-19 symptoms including fatigue and headache. General medical conditions were the sole independent risk factor for any menstrual changes. Metabolomic analysis highlighted disturbances in steroid hormone biosynthesis. We identified 52 significantly differential metabolites between groups with and without any menstrual changes (AnyC vs. NoC), with high discrimination achieved by combining phenylglyoxylic acid, PC O-40, traumatic acid, and estrone sulfate. Furthermore, several significantly upregulated metabolites were closely correlated with estradiol (E2) levels, including estrone sulfate, which was also positively correlated with T levels. Specifically, T levels decreased with recovery duration in the AnyC group (p = 0.0015). Collectively, our findings uncovered key clinical factors and metabolic disruptions in menstrual changes, underscoring potential adverse long-term effects of COVID-19 on women's health.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256175","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

New Mechanisms and Therapeutic Targets in Systemic Lupus Erythematosus 系统性红斑狼疮的新机制和治疗靶点

IF 10.7

MedComm Pub Date : 2025-06-09 DOI: 10.1002/mco2.70246

Jingru Tian, Hang Zhou, Wei Li, Xu Yao, Qianjin Lu

{"title":"New Mechanisms and Therapeutic Targets in Systemic Lupus Erythematosus","authors":"Jingru Tian, Hang Zhou, Wei Li, Xu Yao, Qianjin Lu","doi":"10.1002/mco2.70246","DOIUrl":"https://doi.org/10.1002/mco2.70246","url":null,"abstract":"Systemic lupus erythematosus (SLE) is a multifaceted dautoimmune disease driven by complex interactions among genetic, environmental, and sex-related factors. Central to its pathogenesis are type I interferons (IFN-I) and autoantibodies that target nucleic acids and nucleic acid-binding proteins. These mediators, often triggered by environmental stimuli in genetically susceptible individuals, promote sustained immune activation and chronic inflammation. Despite advances in understanding the immunological landscape of SLE, the precise initiating triggers and early molecular events remain incompletely defined. Recent studies have highlighted the destabilization of innate immune cells, particularly dendritic cells and monocytes, as critical early events in the pathogenesis of SLE. These alterations precede and potentially initiate the downstream activation of autoreactive lymphocytes. This review provides an updated synthesis of key epidemiological findings, emerging pathogenic mechanisms, potential therapeutic targets, and advances in translational and clinical research. Particular attention is given to recent insights into disease triggers and early pathological processes, especially the destabilization of innate immune cells. By consolidating these advances, this review aims to refine our understanding of the early immune dysregulation in SLE and to support the development of more precise, mechanism-based therapeutic strategies.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244311","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

Glycoprotein Ibα-Dependent Platelet Activation is Essential for Tumor Cell–Platelet Interaction and Experimental Metastasis 糖蛋白bα依赖性血小板活化是肿瘤细胞-血小板相互作用和实验转移的必要条件

IF 10.7

MedComm Pub Date : 2025-06-09 DOI: 10.1002/mco2.70217

Kangxi Zhou, Qing Li, Yue Xia, Chenglin Sun, Jing Wang, Yueyue Sun, Xinxin Ge, Mengnan Yang, Yu Li, Sai Zhang, Lili Zhao, Chunliang Liu, Khan Muhammad Shoaib, Weiling Xiao, Renping Hu, Kesheng Dai, Rong Yan

{"title":"Glycoprotein Ibα-Dependent Platelet Activation is Essential for Tumor Cell–Platelet Interaction and Experimental Metastasis","authors":"Kangxi Zhou, Qing Li, Yue Xia, Chenglin Sun, Jing Wang, Yueyue Sun, Xinxin Ge, Mengnan Yang, Yu Li, Sai Zhang, Lili Zhao, Chunliang Liu, Khan Muhammad Shoaib, Weiling Xiao, Renping Hu, Kesheng Dai, Rong Yan","doi":"10.1002/mco2.70217","DOIUrl":"https://doi.org/10.1002/mco2.70217","url":null,"abstract":"Metastasis is the main cause of cancer-related deaths and the biggest challenge in improving cancer prognosis. Platelet–tumor cell aggregates are a prerequisite for hematogenous metastasis. However, the internal relation and molecular mechanism of platelets and their receptor glycoprotein (GP) Ibα in platelet–tumor cell interaction and metastasis remain elusive. Here, we find that in the absence of the full-length GPIbα or its cytoplasmic tail, platelets maintain a more resting state and exhibit reduced tumor cell-induced platelet activation. The deficiency of the cytoplasmic tail of GPIbα inhibits tumor cell–platelet interaction, platelet-induced tumor cell migration and invasion, and metastasis. Using a state-of-the-art spinning disk intravital microscopy, we observe a rapid accumulation of platelets on tumor cells, forming numerous tumor cell–platelet aggregates in vivo. We also find that the cytoplasmic tail of GPIbα regulates the tumor cell-induced platelet protein kinase C-α (PKCα) activation, and both the pharmacological inhibition and genetic ablation of platelet PKCα attenuate tumor cell-induced platelet activation, tumor cell–platelet interaction, tumor cell migration and invasion, and metastasis. Overall, our findings reveal for the first time that GPIbα promotes experimental metastasis through its cytoplasmic tail-regulated platelet activation, and suggest a potential target to regulate tumor hematogenous metastasis.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70217","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244641","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

Deep Learning in Digital Breast Tomosynthesis: Current Status, Challenges, and Future Trends 数字乳房断层合成中的深度学习：现状、挑战和未来趋势

IF 10.7

MedComm Pub Date : 2025-06-09 DOI: 10.1002/mco2.70247

Ruoyun Wang, Fanxuan Chen, Haoman Chen, Chenxing Lin, Jincen Shuai, Yutong Wu, Lixiang Ma, Xiaoqu Hu, Min Wu, Jin Wang, Qi Zhao, Jianwei Shuai, Jingye Pan

{"title":"Deep Learning in Digital Breast Tomosynthesis: Current Status, Challenges, and Future Trends","authors":"Ruoyun Wang, Fanxuan Chen, Haoman Chen, Chenxing Lin, Jincen Shuai, Yutong Wu, Lixiang Ma, Xiaoqu Hu, Min Wu, Jin Wang, Qi Zhao, Jianwei Shuai, Jingye Pan","doi":"10.1002/mco2.70247","DOIUrl":"https://doi.org/10.1002/mco2.70247","url":null,"abstract":"The high-resolution three-dimensional (3D) images generated with digital breast tomosynthesis (DBT) in the screening of breast cancer offer new possibilities for early disease diagnosis. Early detection is especially important as the incidence of breast cancer increases. However, DBT also presents challenges in terms of poorer results for dense breasts, increased false positive rates, slightly higher radiation doses, and increased reading times. Deep learning (DL) has been shown to effectively increase the processing efficiency and diagnostic accuracy of DBT images. This article reviews the application and outlook of DL in DBT-based breast cancer screening. First, the fundamentals and challenges of DBT technology are introduced. The applications of DL in DBT are then grouped into three categories: diagnostic classification of breast diseases, lesion segmentation and detection, and medical image generation. Additionally, the current public databases for mammography are summarized in detail. Finally, this paper analyzes the main challenges in the application of DL techniques in DBT, such as the lack of public datasets and model training issues, and proposes possible directions for future research, including large language models, multisource domain transfer, and data augmentation, to encourage innovative applications of DL in medical imaging.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70247","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244640","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

The Nasal–Brain Drug Delivery Route: Mechanisms and Applications to Central Nervous System Diseases 鼻-脑给药途径：中枢神经系统疾病的机制和应用

IF 10.7

MedComm Pub Date : 2025-06-06 DOI: 10.1002/mco2.70213

Yi Qiu, Shiyuan Huang, Li Peng, Li Yang, Guosong Zhang, Tao Liu, Fang Yan, Xi Peng

{"title":"The Nasal–Brain Drug Delivery Route: Mechanisms and Applications to Central Nervous System Diseases","authors":"Yi Qiu, Shiyuan Huang, Li Peng, Li Yang, Guosong Zhang, Tao Liu, Fang Yan, Xi Peng","doi":"10.1002/mco2.70213","DOIUrl":"https://doi.org/10.1002/mco2.70213","url":null,"abstract":"The blood–brain barrier (BBB) is a highly selective and protective barrier that restricts the entry of most therapeutic agents into the central nervous system (CNS), posing a significant challenge for the treatment of CNS diseases. The nose-to-brain drug delivery (NBDD) route has emerged as a promising strategy to bypass the BBB, offering direct, noninvasive, and efficient transport of drugs to the brain. This review begins with a concise overview of the BBB structure and its biofunctions, followed by an in-depth discussion of the mechanisms underlying the nose-to-brain pathway, including the olfactory and trigeminal nerve routes, and respiratory pathway. We further highlight the therapeutic research development of neurodegenerative diseases, acute neurological diseases, brain tumor, and psychiatric disorders when using NBDD drugs encompassing small-molecule drugs, proteins, peptides, nucleic acids, siRNA, and herbal compounds, in which we also introduce innovative delivery systems, including nanocarriers and novel platforms such as exosomes, which enhance drug stability, targeting efficiency, and bioavailability. In addition, we provide a comprehensive overview of recent clinical advancements in therapeutics delivered via the intranasal route for CNS diseases. Finally, we discuss the challenges and future directions of NBDD, emphasizing its potential to transform the treatment landscape for CNS disorders.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70213","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144219854","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

Discovery and Validation of Novel Biomarkers for Colorectal Neoplasia Detection via Plasma Metabolomics 血浆代谢组学检测结直肠癌的新生物标志物的发现和验证

IF 10.7

MedComm Pub Date : 2025-06-06 DOI: 10.1002/mco2.70201

Jianv Huang, Le Wang, Xiang Zhang, Xinyi Liu, Junyan Miao, Yuefan Shen, Chengqu Fu, Xianxiu Ge, Xue Wang, Jiancong Hu, Guanman Li, Yang Sun, Yinglei Miao, Juncheng Dai, Lingbin Du, Hongxia Ma, Guangfu Jin, Ni Li, Lin Miao, Zhibin Hu, Xiaosheng He, Jun Yu, Hongbing Shen, Dong Hang

{"title":"Discovery and Validation of Novel Biomarkers for Colorectal Neoplasia Detection via Plasma Metabolomics","authors":"Jianv Huang, Le Wang, Xiang Zhang, Xinyi Liu, Junyan Miao, Yuefan Shen, Chengqu Fu, Xianxiu Ge, Xue Wang, Jiancong Hu, Guanman Li, Yang Sun, Yinglei Miao, Juncheng Dai, Lingbin Du, Hongxia Ma, Guangfu Jin, Ni Li, Lin Miao, Zhibin Hu, Xiaosheng He, Jun Yu, Hongbing Shen, Dong Hang","doi":"10.1002/mco2.70201","DOIUrl":"https://doi.org/10.1002/mco2.70201","url":null,"abstract":"Metabolic disturbance plays a critical role in the initiation of colorectal cancer (CRC), yet the identification of metabolites that are useful for early detection of CRC and its precursor lesions remains elusive. We conducted an untargeted plasma metabolomic profiling by liquid chromatography-mass spectrometry in a two-stage case–control study, including 219 CRC cases, 164 colorectal adenoma (CRA) cases, and 219 normal controls (NC) as a training set, and 91 CRC, 115 CRA, and 109 NC as a validation set. Among 891 named metabolites, 239 were significantly altered in CRC versus NC, 26 in CRA versus NC, and 88 in CRC versus CRA within the training set. The results were stable when adjusting for potential confounders. A panel of 10 metabolites, including six lipid species, one benzenoid, one organoheterocyclic compound, one organic acid derivative, and one organic oxygen compound, showed optimal performance in discriminating CRC from NC (AUC = 0.81) in the validation. Moreover, a panel of seven metabolites exhibited optimal performance in discriminating CRA from NC, with an AUC of 0.89. Our findings provide novel evidence supporting specific plasma metabolites, particularly those implicated in lipid metabolism, as promising biomarkers for the early detection of CRC.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144220425","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

Long Noncoding RNA Interleukin 6 Antisense RNA 1 Promotes Inflammatory Effects in Lung Macrophages via Exosomes Through the S100A9/TLR4 Pathway in Chronic Obstructive Pulmonary Disease Progression 长链非编码RNA白介素6反义RNA 1通过外泌体在慢性阻塞性肺疾病进展中通过S100A9/TLR4途径促进肺巨噬细胞的炎症作用

IF 10.7

MedComm Pub Date : 2025-06-06 DOI: 10.1002/mco2.70204

Erkang Yi, Xiaoyu Wang, Yu Liu, Zihui Wang, Ge Bai, Xinyue Mei, Fan Wu, Chengshu Xie, QiYang Li, Weitao Cao, Huahua Xu, Xinyuan Liu, Jieda Cui, Haiqing Li, Ruiting Sun, Xinru Ran, Wei Hong, Zhishan Deng, Bing Li, Yumin Zhou, Pixin Ran

{"title":"Long Noncoding RNA Interleukin 6 Antisense RNA 1 Promotes Inflammatory Effects in Lung Macrophages via Exosomes Through the S100A9/TLR4 Pathway in Chronic Obstructive Pulmonary Disease Progression","authors":"Erkang Yi, Xiaoyu Wang, Yu Liu, Zihui Wang, Ge Bai, Xinyue Mei, Fan Wu, Chengshu Xie, QiYang Li, Weitao Cao, Huahua Xu, Xinyuan Liu, Jieda Cui, Haiqing Li, Ruiting Sun, Xinru Ran, Wei Hong, Zhishan Deng, Bing Li, Yumin Zhou, Pixin Ran","doi":"10.1002/mco2.70204","DOIUrl":"https://doi.org/10.1002/mco2.70204","url":null,"abstract":"This study investigates the role of interleukin 6 antisense RNA 1 (IL6-AS1), a highly expressed long noncoding RNA (lncRNA), in chronic obstructive pulmonary disease (COPD). An adeno-associated virus (AAV) was used to induce the expression of IL6-AS1 in mice, and they were exposed to cigarette smoke to establish a COPD model. IL6-AS1-overexpressing mice exposed to cigarette smoke demonstrated exacerbated COPD-like pathologies. Integrated with single-cell RNA sequencing analysis of COPD patients and pulmonary fibroblast–macrophage coculture system, our findings indicate that the upregulation of IL6-AS1 in fibroblasts enhances the interaction between the S100A9 protein and the AGER and TLR4 receptors on lung macrophages, thereby exacerbating pulmonary inflammation. The molecular mechanism likely involves exosome-mediated secretion, with IL6-AS1 binding to S100A9 protein. These findings suggest that IL6-AS1 may facilitate crosstalk between fibroblasts and macrophages, contributing to increased pulmonary inflammation, an effect that can be blocked by paquinimod. Mendelian randomization analysis further suggests a potential shared causal variant between IL6-AS1 and COPD risk. Taken together, this investigation provides valuable insights into the function of IL6-AS1 and its potential implications for the pathogenesis and therapeutic strategies in COPD.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70204","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144219853","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

Loss of Adenosine Deaminase Acting on RNA 1 Induces Panoptosis and Immune Response in Ulcerative Colitis Gut Mucosa 作用于RNA 1的腺苷脱氨酶缺失诱导溃疡性结肠炎肠道黏膜泛凋亡和免疫应答

IF 10.7

MedComm Pub Date : 2025-06-06 DOI: 10.1002/mco2.70212

Andrea Iannucci, Marco Colella, Macarena Quiroga, Rachele Frascatani, Lorenzo Tomassini, Claudia Maresca, Eleonora Franzè, Federica Laudisi, Giuseppe Sica, Irene Marafini, Alessandro Michienzi, Ivan Zanoni, Giovanni Monteleone, Ivan Monteleone

{"title":"Loss of Adenosine Deaminase Acting on RNA 1 Induces Panoptosis and Immune Response in Ulcerative Colitis Gut Mucosa","authors":"Andrea Iannucci, Marco Colella, Macarena Quiroga, Rachele Frascatani, Lorenzo Tomassini, Claudia Maresca, Eleonora Franzè, Federica Laudisi, Giuseppe Sica, Irene Marafini, Alessandro Michienzi, Ivan Zanoni, Giovanni Monteleone, Ivan Monteleone","doi":"10.1002/mco2.70212","DOIUrl":"https://doi.org/10.1002/mco2.70212","url":null,"abstract":"The gut virome is a complex community that exists in equilibrium with the host. Disruptions of this balance could drive the development of inflammatory diseases, such as inflammatory bowel disease (IBD). RNA editing, particularly A-to-I editing by ADAR1, prevents the excessive immune response to viral double strand (ds) RNA. Failure of RNA editing may sustain inflammation and this study explore the role of ADAR1 in IBD. ADAR1 was analyzed in IBD patients and healthy controls (CTR) using western blotting and qPCR. Colonic epithelial cells (HCEC-1CT), ex vivo organ cultures, and colonic organoids were treated poly I:C after ADAR1 silencing with an antisense oligonucleotide (AS). Inflammatory pathways and PANoptosome were measured by western blotting, flow cytometry, and ELISA. The role of ADAR1 was also studied in DSS-colitis model. ADAR1 was significantly reduced in the inflamed epithelium of ulcerative colitis (UC) gut samples. ADAR1 silencing in HCEC-1CT, ex vivo organ cultures or colonic organoids strongly increases the immune response to poly I:C and leads to activation of inflammatory pathways and PANoptosis. Inhibition of gut ADAR1 expression during DSS-colitis exacerbated gut inflammation. JAK inhibition or AhR activation mitigated the immune response that follows ADAR1 silencing. These data suggest that ADAR1 could be involved in IBD inflammation.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70212","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144220423","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

Targeted Lung Premetastasis Niche: Mechanisms, Strategies, and Application 靶向肺转移前生态位：机制、策略和应用

IF 10.7

MedComm Pub Date : 2025-06-03 DOI: 10.1002/mco2.70248

Chenghao Cao, Di Lu, Huigang Li, Shen Pan, Jianyong Zhuo, Zuyuan Lin, Chiyu He, Peiru Zhang, Songmin Ying, Xuyong Wei, Shusen Zheng, Zhe Yang, Xiao Xu

{"title":"Targeted Lung Premetastasis Niche: Mechanisms, Strategies, and Application","authors":"Chenghao Cao, Di Lu, Huigang Li, Shen Pan, Jianyong Zhuo, Zuyuan Lin, Chiyu He, Peiru Zhang, Songmin Ying, Xuyong Wei, Shusen Zheng, Zhe Yang, Xiao Xu","doi":"10.1002/mco2.70248","DOIUrl":"https://doi.org/10.1002/mco2.70248","url":null,"abstract":"Lung metastasis remains a leading cause of cancer mortality, driven not only by primary tumors but crucially by dynamic interactions within the premetastatic niche (PMN). Emerging evidence reveals that organ-specific PMN formation precedes tumor cell arrival, creating an immunosuppressive microenvironment conducive to metastatic colonization. Primary tumor-derived factors interact with lung resident cells, promoting the recruitment of bone marrow-derived cells and creating a favorable microenvironment for the migrating tumor cells. Despite progress, systematic integration of PMN's multilayered regulatory mechanisms—from mechanism to clinical application remains lacking. The review summarizes recent studies investigating the effects of PMN in the entire process of lung metastasis. Our discussion revolves primarily around extracellular vesicles, extracellular matrix remodeling, proinflammation, immunosuppression, angiogenesis, and metabolic reprogramming. We emphasize the impact of various treatment strategies for primary tumors on the PMN in clinical practice, while also summarizing current diagnostic methods and exploring new therapeutic possibilities in the PMN. Finally, we propose a roadmap for future investigations into the lung PMN, highlighting prioritized research axes that bridge mechanistic discoveries with bench-to-bedside translation of PMN-targeted interventions.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70248","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144206381","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

Persistent Activation of Sphingosine-1-Phosphate Receptor 1 by Phytosphingosine-3,4-Cyclic Phosphate Ameliorates Sepsis by Inhibiting Hyperinflammation and Vascular Hyperpermeability 鞘氨醇-3,4-环磷酸持续激活鞘氨醇-1-磷酸受体1通过抑制高炎症和血管高通透性改善脓毒症

IF 10.7

MedComm Pub Date : 2025-06-03 DOI: 10.1002/mco2.70238

Suhong Duan, Seung-Gook Kim, Jiaying Bao, Hyung-Jin Lim, Joon Woo Kim, Sung-Il Yoon, Young Jun Park, Sanuk Yun, Kye-Seong Kim, Hwa-Ryung Song, Myeong Jun Choi, Myung-Kwan Han

{"title":"Persistent Activation of Sphingosine-1-Phosphate Receptor 1 by Phytosphingosine-3,4-Cyclic Phosphate Ameliorates Sepsis by Inhibiting Hyperinflammation and Vascular Hyperpermeability","authors":"Suhong Duan, Seung-Gook Kim, Jiaying Bao, Hyung-Jin Lim, Joon Woo Kim, Sung-Il Yoon, Young Jun Park, Sanuk Yun, Kye-Seong Kim, Hwa-Ryung Song, Myeong Jun Choi, Myung-Kwan Han","doi":"10.1002/mco2.70238","DOIUrl":"https://doi.org/10.1002/mco2.70238","url":null,"abstract":"Sepsis is a life-threatening disease characterized by multiorgan dysfunction caused by an abnormal immune response to microbial infection. Sphingosine-1-phosphate (S1P) levels are significantly lower in patients with sepsis and are negatively correlated with the severity of sepsis. However, whether the S1P signaling pathway is a target for sepsis treatment remains unknown. Here, we show that our newly synthesized phytosphingosine-3,4-cyclic phosphate (3,4-cPP), a functional agonist of S1P receptor 1 (S1P1), exerts a strong protective effect against severe cecal ligation and puncture (CLP)-induced sepsis. 3,4-cPP persistently activates S1P1 without inducing internalization. 3,4-cPP upregulates SIRT1 expression in macrophages and endothelial cells via S1P1 activation. Additionally, 3,4-cPP decreases serum levels of proinflammatory cytokines, including IL-6 and TNF-α, and inhibits endothelial permeability in CLP-induced septic mice. Conditional knockout of SIRT1, an NAD+-dependent deacetylase, in macrophages or endothelial cells counteracts the inhibition of inflammatory cytokine secretion and prevention of endothelial cell permeability by 3,4-cPP in CLP-induced septic mice, indicating that the S1P1/SIRT1 axis in both the endothelium and macrophages is essential for survival in sepsis. Collectively, the data suggest that prolonged activation of the S1P1/SIRT1 signaling pathway protects against sepsis by inhibiting hyperinflammation and vascular hyperpermeability.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70238","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144206324","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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