iMeta最新文献

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":""},"PeriodicalIF":23.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148095947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":""},"PeriodicalIF":23.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148095948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intratumoral <i>Enterobacter hormaechei</i> drives gemcitabine resistance in pancreatic cancer via <i>cdd</i> _L-mediated drug inactivation.","authors":"Jun-Feng Peng, Meixia Li, Ting Niu, Judong Li, Wei Niu, Minghui Zheng, Quanjiang Ji, Chuan Li, Chenghao Shao, Kan Ding","doi":"10.1002/imt2.70126","DOIUrl":"10.1002/imt2.70126","url":null,"abstract":"<p><p>Gemcitabine resistance poses a critical barrier to improving survival in pancreatic cancer, yet the microbial drivers remain elusive. By integrating 16S rRNA amplicon sequencing with large-scale culturomics across 114 clinical samples, we identified <i>Enterobacter hormaechei</i> as a key intratumoral pathogen. We demonstrate that <i>E. hormaechei</i> confers resistance by enzymatically converting the drug to its inactive metabolite dFdU via a unique long-isoform cytidine deaminase encoded by <i>cdd</i> _L. Kinetic analysis revealed exceptional catalytic efficiency (<i>K</i> _m = 0.22 mM, <i>k</i> _cat = 194.05 s^-1), and genetic ablation of <i>cdd</i> _L fully restored drug sensitivity. In vivo, antibiotic co-treatment eliminated intratumoral bacteria and potentiated gemcitabine efficacy, enabling a 50% dosage reduction without comprising therapeutic outcome. Pan-cancer analysis further confirmed the broad prevalence of <i>Enterobacter</i> across multiple solid tumor types. These findings elucidate a <i>cdd</i> _L-mediated mechanism of chemoresistance and identify intratumoral <i>E. hormaechei</i> as a tractable therapeutic target for optimizing gemcitabine-based regimens and improving patient outcomes.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":"e70126"},"PeriodicalIF":44.4,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847010","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":""},"PeriodicalIF":23.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148085600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptomics reveals cellular heterogeneity and phenotypic transitions of smooth muscle cells in aortic dissection.","authors":"Liang Shao, Fan Hu, Ling-Na Zhao, Jian-Ping Luo, Peng-Tao Zou, Xiu Liu, Shao-Yi Zheng, Cong Chen, Lin-Xiong Ye, Yu-Xuan Zhou, Jiaqi Zhang, Kaidi Jin, Ping Zhang","doi":"10.1002/imt2.70124","DOIUrl":"10.1002/imt2.70124","url":null,"abstract":"<p><p>We utilized single-cell RNA sequencing (scRNA-seq) to investigate cellular heterogeneity and signaling networks in aortic dissection (AD) tissues compared to adjacent normal tissues. The analysis identified five smooth muscle cell (SMC) subtypes, with SMC2 linked to fibrosis and SMC3 associated with inflammation. Thrombus-positive AD samples showed upregulated angiopoietin-like 4 (<i>ANGPTL4</i>) and increased M2 macrophages, indicating an immunosuppressive microenvironment. Cell-cell communication analysis revealed a shift in vascular endothelial growth factor A (<i>VEGFA</i>) signaling from SMCs to fibroblasts, disrupting vascular homeostasis. In vitro experiments confirmed SMC2-induced endothelial-to-mesenchymal transition and SMC3-driven inflammatory responses via mitogen-activated protein kinase (MAPK) pathways. Immunofluorescence validated elevated insulin-like growth factor binding protein 2 (<i>IGFBP2</i>), procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (<i>PLOD2</i>), and <i>VEGFA</i> in AD tissues, supporting their roles in matrix remodeling and angiogenesis. These findings highlight SMC phenotypic switching and altered <i>VEGFA</i> signaling as key drivers of AD, proposing novel therapeutic targets to restore vascular integrity.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":"e70124"},"PeriodicalIF":44.4,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847032","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":""},"PeriodicalIF":23.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148062236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two stable gut microbiome guilds predict liver tumor class and treatment responses.","authors":"Yang Liu, Zefan Zhang, Guojun Wu, Bowen Li, Linghua Wang, Jincheng Wang, Zixian Wei, Zhiyue Wang, Jinhua Yang, Kunyu Zhang, Tianqi Zhang, Xin Tao, Tao Chen, Jia Fan, Jian Zhou, Xinrong Yang, Liping Zhao, Yunwei Wei","doi":"10.1002/imt2.70123","DOIUrl":"10.1002/imt2.70123","url":null,"abstract":"<p><p>Gut microbiome alterations are increasingly associated with hepatocellular carcinoma (HCC), highlighting the gut-liver axis as a key contributor to tumor progression and prognosis. Taxon-based HCC microbiome studies have shown limited reproducibility because they are affected by database dependency, taxonomic ambiguity, and overlooked ecological interactions. The Two Competing Guilds (TCG) model, based on stable gut microbiome interactions, provides a structurally grounded framework for robust, generalizable biomarkers. Using shotgun metagenomic data from a newly recruited cohort of 120 surgically resectable HCC cases and 76 benign liver tumor controls, we constructed co-abundance networks to identify stably correlated genome pairs and assembled a hepatic cancer-TCG (HCC-TCG) model composed of 142 genomes. Functionally, one Guild had more genes for butyrate production from carbohydrate fermentation while the other Guild was enriched in genes for virulence factors and antibiotic resistance, highlighting its potential proinflammatory roles. Classifiers trained on the abundance profiles of HCC-TCG genomes successfully distinguished HCC from benign liver tumors (area under the receiver operating characteristic, AUROC = 0.70) and from colorectal liver metastases (CRLM) (AUROC = 0.78). In an external validation cohort, the model further discriminated against HCC from intrahepatic cholangiocarcinoma (iCCA) (AUROC  =  0.72), and from healthy controls (AUROC  =  0.79-0.85), demonstrating its broad applicability for tumor stratification across clinical contexts. Moreover, HCC-TCG profiles predicted post-resection recurrence risk and response to adjuvant therapies (AUROC up to 0.83). Importantly, external validation in two independent cohorts of advanced HCC patients treated with PD-1/PD-L1 inhibitors demonstrated consistent predictive performance (AUROC  =  0.64-0.73), confirming the model's generalizability in nonsurgical and immunotherapy contexts. This genome-specific, ecologically structured, and database-independent framework identifies a conserved Guild-based microbiome signature for HCC. Our findings demonstrate that a fixed genome-resolved ecological structure retains transferable discriminatory signal across clinical contexts. The HCC-TCG framework provides a genome-specific, interaction-based foundation for future development of non-invasive microbiome stratification strategies requiring prospective validation.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":"e70123"},"PeriodicalIF":44.4,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147846967","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":""},"PeriodicalIF":23.7,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148094336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A large-scale single-cell transcriptomic atlas indicates the immune panorama of influenza A infection.","authors":"Yi Wang, Shuzi Liu, Laurence Don Wai Luu, Yongzhi Zhai, Chenliang Zhu, Zhaomin Feng, Yao Tan, Linglong Wan, Jie Wang, Juan Zhou, Jing Wang, Lixin Xie, Quanyi Wang, Fei Xie","doi":"10.1002/imt2.70121","DOIUrl":"10.1002/imt2.70121","url":null,"abstract":"<p><p>Influenza A virus (IAV) infection has a wide clinical spectrum, from mild illness to life-threatening pneumonia, yet the underlying immune determinants of disease remain poorly defined. Here, we generated a large-scale single-cell transcriptomic atlas from peripheral blood, profiling more than 612,010 cells from 97 individuals, including healthy controls, and patients with mild, severe, or convalescent IAV infection. Our findings uncovered a core immune dichotomy that determines clinical severity: a protective, monocyte-centric antiviral state in mild disease versus a pathological, neutrophil- and myeloid-derived suppressor cell (MDSC)-driven hyperinflammatory state in severe infection. Severe disease was marked by a peripheral hyperinflammatory state, driven by specific monocyte and neutrophil subsets via the <i>S100A8</i>/<i>9</i>/12-<i>TLR4</i>/<i>RAGE</i> signaling axis, and was coupled with the expansion of granulocytic MDSCs that likely contribute to T cell paralysis. In contrast, mild disease was associated with a protective, monocyte-centric response characterized by robust antiviral interferon signaling and enhanced antigen presentation. This functional divergence extends to the adaptive immune system, where mild disease was associated with CD8⁺ T cells displaying a balance of high cytotoxicity and regulated exhaustion. In severe illness, however, T cells become profoundly dysfunctional, exhibiting signatures of metabolic stress and apoptosis alongside the emergence of pathogenic, pro-inflammatory regulatory T cells. Together, our atlas provides a high-resolution immunological blueprint of human IAV infection, delineates the cellular states and pathways that govern clinical trajectories and offers a critical resource for developing host-directed therapies.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":"e70121"},"PeriodicalIF":44.4,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147846957","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}

{"title":"A bioactive ginsenoside alleviates hepatocellular ferroptosis induced by oxidized phospholipid accumulation in nonalcoholic steatohepatitis","authors":"Yibo Zong,&nbsp;Guo Long,&nbsp;Tiantian Gu,&nbsp;Pan Huang,&nbsp;Yong Tian,&nbsp;Wenwu Xu,&nbsp;Xiheng Hu,&nbsp;Dazun Shi,&nbsp;Lizhi Lu,&nbsp;Tao Zeng","doi":"10.1002/imt2.70114","DOIUrl":"https://doi.org/10.1002/imt2.70114","url":null,"abstract":"<p>Schematic representation showing that 20 (S)-Rg3 improves mouse NASH. 20(S)-Rg3 reduces OxPLs levels and ameliorates ferroptosis in the liver of NASH mice. Mechanistically, 20(S)-Rg3 activates SPOP. Meanwhile, SPOP attenuates the ATF3-mediated transcriptional repression of NUPR1 by enhancing the K48-linked ubiquitination of ATF3. Upregulated NUPR1 rescues redox balance and reduces lipid peroxidation, ultimately inhibiting hepatocellular ferroptosis.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 1","pages":""},"PeriodicalIF":23.7,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70114","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147562648","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}