iMeta最新文献

{"title":"Climate factors drive the local adaptation of Old World cattle","authors":"Luyang Sun,&nbsp;Liangliang Jin,&nbsp;Ting Sun,&nbsp;Chenqi Bian,&nbsp;Fuwen Wang,&nbsp;Shuang Li,&nbsp;Hao Li,&nbsp;Jianyong Liu,&nbsp;Jicai Zhang,&nbsp;Johannes A. Lenstra,&nbsp;Artem Nedoluzhko,&nbsp;Zhuqing Zheng,&nbsp;Ruidong Xiang,&nbsp;Wai Yee Low,&nbsp;Wangdui Basang,&nbsp;Zhuzha Basang,&nbsp;Bin Li,&nbsp;Quji Suolang,&nbsp;Li Zhao,&nbsp;Wangmu Silang,&nbsp;Luobu Ciren,&nbsp;Zhandui Pubu,&nbsp;Qiangma Xire,&nbsp;Yanliang Song,&nbsp;Yuanpeng Gao,&nbsp;Dawei Wei,&nbsp;Rende Song,&nbsp;Min-Sheng Peng,&nbsp;Bizhi Huang,&nbsp;Yun Ma,&nbsp;Xiaoting Xia,&nbsp;Chuzhao Lei,&nbsp;Ningbo Chen","doi":"10.1002/imt2.70108","DOIUrl":"https://doi.org/10.1002/imt2.70108","url":null,"abstract":"<p>Climate adaptation genomics of cattle. We comparatively analyzed genomic data from 85 Old World cattle breeds/populations of Eurasia and Africa to identify genetic factors associated with climate factors. Environmental genome-wide association studies revealed 3165 single-nucleotide polymorphisms (SNPs) with strong correlations between climate factors and allele frequencies. We also identified loci that were significantly associated with temperature factors in the regulatory regions, such as promoter regions, of genes (<i>ANKRD11</i>, <i>RPL13</i>, <i>CDK10</i>, and <i>VPS9D1</i>) under strong selection pressure on <i>Bos taurus</i> autosome 18, which might regulate the expression of these genes. These significantly associated SNPs could be used as potential resources for marker-assisted breeding programs aimed at climate resilience and sustainable cattle production under changing environmental conditions.\u0000\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/imt2.70108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147564394","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":"Oral proton-reprogrammed nanomedicine to break the inflammatory bowel disease-Clostridium difficile infection vicious cycle","authors":"Wensheng Chen,&nbsp;Yuntao Zhang,&nbsp;Jue Wang,&nbsp;Yiming Li,&nbsp;Hao Wu,&nbsp;Qiong Huang,&nbsp;Wei Wu,&nbsp;Kelong Ai","doi":"10.1002/imt2.70112","DOIUrl":"https://doi.org/10.1002/imt2.70112","url":null,"abstract":"<p><i>Clostridium difficile</i> infection (CDI) is a major complication of inflammatory bowel disease (IBD), but the complicated treatment strategy of antimicrobial drugs and immunosuppressive drugs cannot effectively control the syndrome of IBD and CDI. Glycolysis in intestinal epithelial cells (IECs) leads to excessive production of lactic acid, which is considered to be a key factor in the destruction of the intestinal barrier by toxin B of <i>Clostridium difficile</i> (TcdB). In this study, we revealed that uncoupling protein 2 (UCP2) was highly expressed in IECs, and disrupted mitochondrial function to reprogram metabolism toward glycolysis, thereby weakening the resistance of IECs to TcdB. We developed an oral proton-reprogrammed nanomedicine (OPR) to convert the metabolism of IECs from glycolysis to oxidative phosphorylation, which can effectively alleviate IBD and CDI syndromes. OPR blocks the rapid delivery of protons to the mitochondrial matrix induced by UCP2, which restores mitochondrial membrane potential (MMP) and drives protons to reenter the matrix through ATP synthase, mediating the recovery of mitochondrial function. In mouse IBD and IBD complicated CDI (IBD-CDI) models, OPR selectively targeted inflammatory colonic lesions, alleviated mitochondria-dependent pyroptosis of IECs, inhibited macrophage STING pathway activation, and reduced lactic acid levels. Especially in the treatment of IBD-CDI syndrome, the therapeutic effect of OPR is far better than the combination of antibiotics and immunosuppressive drugs. In summary, our study establishes UCP2-mediated mitochondrial disability as a key mechanism for the functioning of TcdB and suggests that IEC metabolic reprogramming could be a therapeutic target.</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/imt2.70112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147567038","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":"Climate factors drive the local adaptation of Old World cattle","authors":"Luyang Sun,&nbsp;Liangliang Jin,&nbsp;Ting Sun,&nbsp;Chenqi Bian,&nbsp;Fuwen Wang,&nbsp;Shuang Li,&nbsp;Hao Li,&nbsp;Jianyong Liu,&nbsp;Jicai Zhang,&nbsp;Johannes A. Lenstra,&nbsp;Artem Nedoluzhko,&nbsp;Zhuqing Zheng,&nbsp;Ruidong Xiang,&nbsp;Wai Yee Low,&nbsp;Wangdui Basang,&nbsp;Zhuzha Basang,&nbsp;Bin Li,&nbsp;Quji Suolang,&nbsp;Li Zhao,&nbsp;Wangmu Silang,&nbsp;Luobu Ciren,&nbsp;Zhandui Pubu,&nbsp;Qiangma Xire,&nbsp;Yanliang Song,&nbsp;Yuanpeng Gao,&nbsp;Dawei Wei,&nbsp;Rende Song,&nbsp;Min-Sheng Peng,&nbsp;Bizhi Huang,&nbsp;Yun Ma,&nbsp;Xiaoting Xia,&nbsp;Chuzhao Lei,&nbsp;Ningbo Chen","doi":"10.1002/imt2.70108","DOIUrl":"https://doi.org/10.1002/imt2.70108","url":null,"abstract":"<p>Climate adaptation genomics of cattle. We comparatively analyzed genomic data from 85 Old World cattle breeds/populations of Eurasia and Africa to identify genetic factors associated with climate factors. Environmental genome-wide association studies revealed 3165 single-nucleotide polymorphisms (SNPs) with strong correlations between climate factors and allele frequencies. We also identified loci that were significantly associated with temperature factors in the regulatory regions, such as promoter regions, of genes (<i>ANKRD11</i>, <i>RPL13</i>, <i>CDK10</i>, and <i>VPS9D1</i>) under strong selection pressure on <i>Bos taurus</i> autosome 18, which might regulate the expression of these genes. These significantly associated SNPs could be used as potential resources for marker-assisted breeding programs aimed at climate resilience and sustainable cattle production under changing environmental conditions.\u0000\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/imt2.70108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147564444","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":"Fast bootstrap and reliable readout using hidden references for DNA data storage","authors":"Weigang Chen,&nbsp;Shuang Liu,&nbsp;Quan Guo,&nbsp;Rui Qin,&nbsp;Qi Ge,&nbsp;Tingting Qi,&nbsp;Yingjin Yuan","doi":"10.1002/imt2.70105","DOIUrl":"https://doi.org/10.1002/imt2.70105","url":null,"abstract":"<p>Data storage using large DNA fragments enables low-cost in vivo replication and offers a promising strategy for distributed data applications. However, data readout from massive, unordered sequencing reads requires alignment based on overlapping regions and is complicated by diverse sequencing errors, especially insertion and deletion (indel) errors. Here, we propose a fast and reliable readout framework in a bootstrap manner tailored for data storage using watermarked large DNA fragments. Our scheme transforms the de novo readout into a resequencing-like workflow through multiple-fold hidden references, substantially reducing readout complexity. The framework is compatible with sequencing platforms exhibiting diverse error profiles. For technologies with low indel rates, we employ correlation-based identification and bit-wise consensus to enable rapid decoding. For indel-prone platforms, we incorporate progressive read alignment using multiple-fold hidden references and the forward-backward algorithm to ensure robust recovery. In vivo experiments on large DNA fragments with different coding efficiencies validated the proposed framework. Error-free recovery was achieved using Illumina reads (raw error rate of ~0.2%) at a coverage of 0.6–2.5× and using nanopore reads (raw error rate ~5%) at a coverage of 1.6× or 4.3×. These results demonstrate the practicality and scalability of large-fragment DNA storage for real-world applications.</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/imt2.70105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147565083","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":"Oral proton-reprogrammed nanomedicine to break the inflammatory bowel disease-Clostridium difficile infection vicious cycle","authors":"Wensheng Chen,&nbsp;Yuntao Zhang,&nbsp;Jue Wang,&nbsp;Yiming Li,&nbsp;Hao Wu,&nbsp;Qiong Huang,&nbsp;Wei Wu,&nbsp;Kelong Ai","doi":"10.1002/imt2.70112","DOIUrl":"https://doi.org/10.1002/imt2.70112","url":null,"abstract":"<p><i>Clostridium difficile</i> infection (CDI) is a major complication of inflammatory bowel disease (IBD), but the complicated treatment strategy of antimicrobial drugs and immunosuppressive drugs cannot effectively control the syndrome of IBD and CDI. Glycolysis in intestinal epithelial cells (IECs) leads to excessive production of lactic acid, which is considered to be a key factor in the destruction of the intestinal barrier by toxin B of <i>Clostridium difficile</i> (TcdB). In this study, we revealed that uncoupling protein 2 (UCP2) was highly expressed in IECs, and disrupted mitochondrial function to reprogram metabolism toward glycolysis, thereby weakening the resistance of IECs to TcdB. We developed an oral proton-reprogrammed nanomedicine (OPR) to convert the metabolism of IECs from glycolysis to oxidative phosphorylation, which can effectively alleviate IBD and CDI syndromes. OPR blocks the rapid delivery of protons to the mitochondrial matrix induced by UCP2, which restores mitochondrial membrane potential (MMP) and drives protons to reenter the matrix through ATP synthase, mediating the recovery of mitochondrial function. In mouse IBD and IBD complicated CDI (IBD-CDI) models, OPR selectively targeted inflammatory colonic lesions, alleviated mitochondria-dependent pyroptosis of IECs, inhibited macrophage STING pathway activation, and reduced lactic acid levels. Especially in the treatment of IBD-CDI syndrome, the therapeutic effect of OPR is far better than the combination of antibiotics and immunosuppressive drugs. In summary, our study establishes UCP2-mediated mitochondrial disability as a key mechanism for the functioning of TcdB and suggests that IEC metabolic reprogramming could be a therapeutic target.</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/imt2.70112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147567291","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":"Curcuminoids amplify host innate antiviral immunity via the CRYAB-RBM26 axis in viral infection","authors":"Tingting Chen,&nbsp;Xiang Wang,&nbsp;Guangyuan Zhang,&nbsp;Lu Wang,&nbsp;Junhao Wan,&nbsp;Lirong Tan,&nbsp;Xinyue Fan,&nbsp;Siqin Meng,&nbsp;Zhixing Jin,&nbsp;Yuzhang Liang,&nbsp;Haoze Li,&nbsp;Ziyuan Wan,&nbsp;Xiaotong Xu,&nbsp;Yan Zhang,&nbsp;Li Qin,&nbsp;Anna Malashicheva,&nbsp;Yu Du,&nbsp;Guangchao Zang,&nbsp;Guixue Wang","doi":"10.1002/imt2.70111","DOIUrl":"https://doi.org/10.1002/imt2.70111","url":null,"abstract":"<p>Curcuminoids, including curcumin (CUR) and demethoxycurcumin (DMC), are known for their antiviral properties, but their underlying antiviral targets remain unclear, and the relationship between curcuminoids and the type I interferon (IFN-I) signaling pathway has not been fully elucidated. Here, we explored the regulatory effects of DMC and CUR on the IFN-I pathway in an EV-D68-infected murine model and employed multiomics analysis to identify key drug targets and their interaction networks. FTIR analysis indicated that DMC has better physicochemical stability than CUR, exhibiting greater stability under changes in light, temperature, and pH. In both in <i>vitro</i> and neonatal mouse models, DMC and CUR effectively inhibited EV-D68 replication by suppressing viral <i>2A</i> gene expression and the release of proinflammatory cytokines. Both compounds upregulated the molecular chaperone CRYAB (αB-crystallin), which translocates to the nucleus and acts as a central regulator of host metabolism and antiviral immunity during EV-D68 infection. Further multiomics analyses revealed that CRYAB overexpression inhibited purine metabolism and upregulated interferon-stimulated genes. Proteomic profiling identified RBM26 as a key CRYAB-interacting target. CRYAB stabilizes RBM26 by inhibiting virus-induced ubiquitination, which leads to enhanced IFN-I responses. DMC and CUR activated the mtDNA-cGAS-STING pathway via RBM26, stimulating downstream signaling and antiviral effects. RBM26 reconstitution altered the splicing of cytidine/uridine monophosphate kinase 2 (<i>CMPK2</i>), resulting in increased nucleotide turnover and reduced cytidine levels, impairing viral replication. DMC/CUR treatment or <i>CRYAB</i> overexpression similarly reduced intracellular cytidine and uridine levels, increasing antiviral activity. Additionally, DMC/CUR restored mtDNA levels suppressed by EV-D68 infection in an RBM26-dependent manner, stimulating cGAS-mediated cGAMP production and activating the STING-TBK1-IRF3 axis. These findings not only clarify the molecular mechanisms underlying the antiviral effects of curcuminoids but also highlight their therapeutic potential as host-directed antiviral agents.</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/imt2.70111","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147568278","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":"Curcuminoids amplify host innate antiviral immunity via the CRYAB-RBM26 axis in viral infection","authors":"Tingting Chen,&nbsp;Xiang Wang,&nbsp;Guangyuan Zhang,&nbsp;Lu Wang,&nbsp;Junhao Wan,&nbsp;Lirong Tan,&nbsp;Xinyue Fan,&nbsp;Siqin Meng,&nbsp;Zhixing Jin,&nbsp;Yuzhang Liang,&nbsp;Haoze Li,&nbsp;Ziyuan Wan,&nbsp;Xiaotong Xu,&nbsp;Yan Zhang,&nbsp;Li Qin,&nbsp;Anna Malashicheva,&nbsp;Yu Du,&nbsp;Guangchao Zang,&nbsp;Guixue Wang","doi":"10.1002/imt2.70111","DOIUrl":"https://doi.org/10.1002/imt2.70111","url":null,"abstract":"<p>Curcuminoids, including curcumin (CUR) and demethoxycurcumin (DMC), are known for their antiviral properties, but their underlying antiviral targets remain unclear, and the relationship between curcuminoids and the type I interferon (IFN-I) signaling pathway has not been fully elucidated. Here, we explored the regulatory effects of DMC and CUR on the IFN-I pathway in an EV-D68-infected murine model and employed multiomics analysis to identify key drug targets and their interaction networks. FTIR analysis indicated that DMC has better physicochemical stability than CUR, exhibiting greater stability under changes in light, temperature, and pH. In both in <i>vitro</i> and neonatal mouse models, DMC and CUR effectively inhibited EV-D68 replication by suppressing viral <i>2A</i> gene expression and the release of proinflammatory cytokines. Both compounds upregulated the molecular chaperone CRYAB (αB-crystallin), which translocates to the nucleus and acts as a central regulator of host metabolism and antiviral immunity during EV-D68 infection. Further multiomics analyses revealed that CRYAB overexpression inhibited purine metabolism and upregulated interferon-stimulated genes. Proteomic profiling identified RBM26 as a key CRYAB-interacting target. CRYAB stabilizes RBM26 by inhibiting virus-induced ubiquitination, which leads to enhanced IFN-I responses. DMC and CUR activated the mtDNA-cGAS-STING pathway via RBM26, stimulating downstream signaling and antiviral effects. RBM26 reconstitution altered the splicing of cytidine/uridine monophosphate kinase 2 (<i>CMPK2</i>), resulting in increased nucleotide turnover and reduced cytidine levels, impairing viral replication. DMC/CUR treatment or <i>CRYAB</i> overexpression similarly reduced intracellular cytidine and uridine levels, increasing antiviral activity. Additionally, DMC/CUR restored mtDNA levels suppressed by EV-D68 infection in an RBM26-dependent manner, stimulating cGAS-mediated cGAMP production and activating the STING-TBK1-IRF3 axis. These findings not only clarify the molecular mechanisms underlying the antiviral effects of curcuminoids but also highlight their therapeutic potential as host-directed antiviral agents.</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/imt2.70111","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147568283","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":"BIOME cohort: Multi-system microbiome dynamics and clinical outcomes in massive burn injury patients","authors":"Runzhi Huang,&nbsp;Yixu Li,&nbsp;Xiaoliang Li,&nbsp;Xulin Chen,&nbsp;Gang Xu,&nbsp;Shurun Huang,&nbsp;Weixi Yang,&nbsp;Xiaodong Li,&nbsp;Haiming Xin,&nbsp;Jianqiang Jiao,&nbsp;Hui Chen,&nbsp;Yuguo Xie,&nbsp;Peng Duan,&nbsp;Wenjun Liu,&nbsp;Xiangdong Deng,&nbsp;Zongyu Li,&nbsp;Yiping Xiu,&nbsp;Jiansheng Zheng,&nbsp;Rujun Chen,&nbsp;Zhaohong Chen,&nbsp;Xingang Wang,&nbsp;Xiaojian Li,&nbsp;Gaoxing Luo,&nbsp;Yi Zhang,&nbsp;Hongyan Zhang,&nbsp;Shichu Xiao,&nbsp;Liang Xiao,&nbsp;Ruijin Guo,&nbsp;Jie Zhang,&nbsp;Xiaofei Ye,&nbsp;Hongtai Tang,&nbsp;Qiao Zuo,&nbsp;Bin Qu,&nbsp;Bingwei Sun,&nbsp;Changhong Lu,&nbsp;Chengliang Deng,&nbsp;Deyi Zheng,&nbsp;Geng Ji,&nbsp;Haisheng Li,&nbsp;Haizhou Yu,&nbsp;Hua Zhou,&nbsp;Jian Wu,&nbsp;Lanjun Nie,&nbsp;Lei Wang,&nbsp;Pihong Zhang,&nbsp;Qingfu Zhang,&nbsp;Shengwu Chao,&nbsp;Sisi Yang,&nbsp;Xianglin Ding,&nbsp;Xiangsheng Ding,&nbsp;Ying Yan,&nbsp;Jiangyong Shen,&nbsp;Yongjian Zhao,&nbsp;Yunchuan Pan,&nbsp;Yunbiao Shen,&nbsp;Yu Zhang,&nbsp;Zhihui Yao,&nbsp;Zhe Cheng,&nbsp;Jiangfan Xie,&nbsp;Zhigang Chu,&nbsp;Shijie Li,&nbsp;Long Xu,&nbsp;Xiuming Yang,&nbsp;Sujie Xie,&nbsp;Hanlin Sun,&nbsp;Shuyuan Xian,&nbsp;Dezhi Han,&nbsp;Maolong Dong,&nbsp;Chengde Xia,&nbsp;Peng Luo,&nbsp;Yongming Yao,&nbsp;Zhaofan Xia,&nbsp;Shizhao Ji","doi":"10.1002/imt2.70106","DOIUrl":"https://doi.org/10.1002/imt2.70106","url":null,"abstract":"<p>Massive burn injuries (MBIs) are associated with high mortality and disability rates, primarily due to microbial-driven sepsis from extensive skin barrier loss and subsequent scar formation. This makes MBI a compelling model for studying multi-system microbial dysbiosis following skin barrier destruction. We launched the Burn &amp; Trauma Injury Organisms and Microbiome Ecology (BIOME) project, planning to enroll at least 150 MBI patients from 50 hospitals across 28 provinces, autonomous regions, and municipalities in China. The cohort includes skin swabs, intestinal and oral samples, and longitudinal clinical data collected from within 72 h post-injury through 1 year of follow-up. This multicenter, prospective, longitudinal cohort will establish a comprehensive clinical microbiota resource for patients with MBI. By integrating multi-system microbiome profiling with clinical outcomes, the BIOME project aims to elucidate the translational role of microbiota reconstruction as a potential target for diagnosis, prognosis, and therapeutic intervention in severe burn care.\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/imt2.70106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147570162","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":"Nano-plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction","authors":"Yi Zhang,&nbsp;Zheng Lin,&nbsp;Runtong Huang,&nbsp;Yang Zhang,&nbsp;Lei Wang,&nbsp;Zan Fu,&nbsp;Chao Wang,&nbsp;Shuai Xiao,&nbsp;Heru Pramono,&nbsp;Kui Xu,&nbsp;Zhimin Xu,&nbsp;Yulong Yin","doi":"10.1002/imt2.70103","DOIUrl":"https://doi.org/10.1002/imt2.70103","url":null,"abstract":"<p>The pervasiveness of microplastic pollution poses a growing health risk, yet its long-term metabolic consequences remain poorly defined. Here, we exposed mice to polyethylene terephthalate nanoparticle (NP) and combined histopathology, biochemistry, metabolomics, and metagenomics to resolve their interactions. NP ingestion induced a severe systemic phenotype characterized by weight loss, organ atrophy, dyslipidemia, and gut barrier collapse. Mechanistically, NPs disrupted bile acid (BA) homeostasis by hyperactivating hepatic synthesis pathways while suppressing microbial 7α-dehydroxylation. This accumulation of cytotoxic BAs drove hepatic lipogenesis and aggravated mucosal inflammation. Crucially, metagenomics uncovered significant gut microbiota dysbiosis, where the enrichment of bile salt hydrolase-encoding taxa and depletion of 7α-dehydroxylating clades reinforced this BA imbalance. Furthermore, the microbiota exhibited functional deterioration, shifting toward glycan degradation with a concurrent loss of antibiotic resistance genes, signaling reduced ecological resilience. These findings identify BA dysregulation and specific microbiota functional losses as primary drivers of NP-induced systemic metabolic collapse.\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/imt2.70103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147570252","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":"Spatial multi-omics identifies a NOTCH3-mediated capillary-mCAF crosstalk driving immune exclusion in hepatocellular carcinoma.","authors":"Fansen Ji, Haochen Li, Qi Wang, Xiaojuan Wang, Jiawei Zhang, Ying Xiao, Huan Li, Hao Liu, Tanqing Long, Boyang Wu, Hao Chen, Haoming Xia, Xinquan Liu, Chuanrui Xu, Yibo Gao, Bingjun Tang, Juan Liu, Shizhong Yang, Jiahong Dong","doi":"10.1002/imt2.70117","DOIUrl":"10.1002/imt2.70117","url":null,"abstract":"<p><p>Fibrosis induced immune exclusion is a hepatocellular carcinoma (HCC) hallmark, underscoring the key role of cancer-associated fibroblasts (CAFs) in immune regulation. Through HCC spatial multi-omics data and integrating pan-cancer scRNA-seq profiles of CAFs under immune checkpoint blockade (ICB) treatment, we characterized a potential crosstalk between capillaries and CAFs mediated by the NOTCH signaling pathway. Specifically, endothelial DLL4-NOTCH3 signaling appears to be associated with matrix-producing CAFs (mCAFs) polarization, leading to extracellular matrix remodeling and the establishment of immune-restrictive niches that hinder T cell infiltration. Perturbation of NOTCH signaling attenuated mCAF differentiation and enhanced T cell infiltration in vitro, and was associated with improved ICB response in both spontaneous and orthotopic HCC mouse models. Collectively, our findings suggest that capillary-mCAFs communication through the NOTCH pathway, particularly <i>NOTCH3</i> activation, may contribute to fibrosis-driven immune exclusion in HCC. Targeting this axis could provide a promising strategy to alleviate stromal barriers and potentiate immunotherapy efficacy.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"5 2","pages":"e70117"},"PeriodicalIF":44.4,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847038","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}