{"title":"Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation","authors":"Weijie Wu, Wenhai Sui, Sizhe Chen, Ziheng Guo, Xu Jing, Xiaolu Wang, Qun Wang, Xinshuang Yu, Wenjing Xiong, Jiansong Ji, Libo Yang, Yuan Zhang, Wenjing Jiang, Guohua Yu, Shuzhen Liu, Wei Tao, Chen Zhao, Yun Zhang, Yuguo Chen, Cheng Zhang, Yihai Cao","doi":"10.1016/j.cmet.2025.01.006","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.006","url":null,"abstract":"Consumption of artificial sweeteners (ASWs) in various foods and beverages has been linked to an increased risk of cardiovascular diseases (CVDs). However, molecular mechanisms underlying ASW-associated CVD remain unknown. Here, we show that consumption of 0.15% aspartame (APM) markedly increased insulin secretion in mice and monkeys. Bilateral subdiaphragmatic vagotomy (SDV) obliterated APM-elevated blood insulin levels, demonstrating crucial roles of parasympathetic activation in regulation of insulin secretion. Incessant APM feeding of ApoE<sup>−/</sup><sup>−</sup> mice aggravated atherosclerotic plaque formation and growth via an insulin-dependent mechanism. Implantation of an insulin-slow-release pump in ApoE<sup>−/−</sup> mice exacerbated atherosclerosis. Whole-genome expression profiling discovered that CX3CL1 chemokine was the most upregulated gene in the insulin-stimulated arterial endothelial cells. Specific deletion of a CX3CL1 receptor, <em>Cx3cr1</em> gene, in monocytes/macrophages completely abrogated the APM-exacerbated atherosclerosis. Our findings uncover a novel mechanism of APM-associated atherosclerosis and therapeutic targeting of the endothelial CX3CL1-macrophage CX3CR1 signaling axis provides an approach for treating atherosclerotic CVD.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"2 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-17DOI: 10.1016/j.cmet.2025.01.013
Phillip A. Dumesic, Sarah E. Wilensky, Symanthika Bose, Jonathan G. Van Vranken, Steven P. Gygi, Bruce M. Spiegelman
{"title":"RBM43 controls PGC1α translation and a PGC1α-STING signaling axis","authors":"Phillip A. Dumesic, Sarah E. Wilensky, Symanthika Bose, Jonathan G. Van Vranken, Steven P. Gygi, Bruce M. Spiegelman","doi":"10.1016/j.cmet.2025.01.013","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.013","url":null,"abstract":"Obesity is associated with systemic inflammation that impairs mitochondrial function. This disruption curtails oxidative metabolism, limiting adipocyte lipid metabolism and thermogenesis, a metabolically beneficial program that dissipates chemical energy as heat. Here, we show that PGC1α, a key governor of mitochondrial biogenesis, is negatively regulated at the level of its mRNA translation by the RNA-binding protein RBM43. RBM43 is induced by inflammatory cytokines and suppresses mitochondrial biogenesis in a PGC1α-dependent manner. In mice, adipocyte-selective <em>Rbm43</em> disruption elevates PGC1α translation and oxidative metabolism. In obesity, <em>Rbm43</em> loss improves glucose tolerance, reduces adipose inflammation, and suppresses activation of the innate immune sensor cGAS-STING in adipocytes. We further identify a role for PGC1α in safeguarding against cytoplasmic accumulation of mitochondrial DNA, a cGAS ligand. The action of RBM43 defines a translational regulatory axis by which inflammatory signals dictate cellular energy metabolism and contribute to metabolic disease pathogenesis.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"64 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-17DOI: 10.1016/j.cmet.2025.01.024
Hans-Georg Sprenger, Melanie J. Mittenbühler, Yizhi Sun, Jonathan G. Van Vranken, Sebastian Schindler, Abhilash Jayaraj, Sumeet A. Khetarpal, Amanda L. Smythers, Ariana Vargas-Castillo, Anna M. Puszynska, Jessica B. Spinelli, Andrea Armani, Tenzin Kunchok, Birgitta Ryback, Hyuk-Soo Seo, Kijun Song, Luke Sebastian, Coby O’Young, Chelsea Braithwaite, Sirano Dhe-Paganon, Bruce M. Spiegelman
{"title":"Ergothioneine controls mitochondrial function and exercise performance via direct activation of MPST","authors":"Hans-Georg Sprenger, Melanie J. Mittenbühler, Yizhi Sun, Jonathan G. Van Vranken, Sebastian Schindler, Abhilash Jayaraj, Sumeet A. Khetarpal, Amanda L. Smythers, Ariana Vargas-Castillo, Anna M. Puszynska, Jessica B. Spinelli, Andrea Armani, Tenzin Kunchok, Birgitta Ryback, Hyuk-Soo Seo, Kijun Song, Luke Sebastian, Coby O’Young, Chelsea Braithwaite, Sirano Dhe-Paganon, Bruce M. Spiegelman","doi":"10.1016/j.cmet.2025.01.024","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.024","url":null,"abstract":"Ergothioneine (EGT) is a diet-derived, atypical amino acid that accumulates to high levels in human tissues. Reduced EGT levels have been linked to age-related disorders, including neurodegenerative and cardiovascular diseases, while EGT supplementation is protective in a broad range of disease and aging models. Despite these promising data, the direct and physiologically relevant molecular target of EGT has remained elusive. Here, we use a systematic approach to identify how mitochondria remodel their metabolome in response to exercise training. From these data, we find that EGT accumulates in muscle mitochondria upon exercise training. Proteome-wide thermal stability studies identify 3-mercaptopyruvate sulfurtransferase (MPST) as a direct molecular target of EGT; EGT binds to and activates MPST, thereby boosting mitochondrial respiration and exercise training performance in mice. Together, these data identify the first physiologically relevant EGT target and establish the EGT-MPST axis as a molecular mechanism for regulating mitochondrial function and exercise performance.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"10 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-11DOI: 10.1016/j.cmet.2025.01.009
Jia Li, Chaoqun Cai, Wei Wen Teo, Kai Shin Chin, Yadanar Than Naing, Shengren Song, Franklin Nelson, Li Qiang, Dan Xu, Lei Sun
{"title":"Isoform usage as a distinct regulatory layer driving nutrient-responsive metabolic adaptation","authors":"Jia Li, Chaoqun Cai, Wei Wen Teo, Kai Shin Chin, Yadanar Than Naing, Shengren Song, Franklin Nelson, Li Qiang, Dan Xu, Lei Sun","doi":"10.1016/j.cmet.2025.01.009","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.009","url":null,"abstract":"Transcriptome modulation is essential for metabolic adaptation to nutrient environments. However, the role of isoform usage, a crucial transcriptome component, is not yet fully understood. This study outlines the landscape of isoform-usage modulations across major metabolic organs in both mice and monkeys, spanning diverse metabolic states. Our in-depth analysis identifies numerous isoform-usage events, intricately influenced by nutrient challenges and largely independent of gene expression regulation. Comparative analyses of mice and monkeys highlight hundreds of conserved isoform events that exhibit consistent responses to nutrient challenges across species and correlate with human metabolic traits. When analyzing splicing factor-binding motifs in nutrient-regulated events, HuR emerges as the predominant orchestrator of the isoform network in adipocytes, which is validated using an adipose tissue-specific knockout and an Ap2-promoter-driven transgenic mouse model. In summary, our results offer a comprehensive perspective on isoform usage in metabolic regulation, setting a platform for future functional inquiries.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"1 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143385071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-10DOI: 10.1016/j.cmet.2025.01.002
Nguyen T.B. Nguyen, Sira Gevers, Rutger N.U. Kok, Lotte M. Burgering, Hannah Neikes, Ninouk Akkerman, Max A. Betjes, Marlies C. Ludikhuize, Can Gulersonmez, Edwin C.A. Stigter, Yvonne Vercoulen, Jarno Drost, Hans Clevers, Michiel Vermeulen, Jeroen S. van Zon, Sander J. Tans, Boudewijn M.T. Burgering, Maria J. Rodríguez Colman
{"title":"Lactate controls cancer stemness and plasticity through epigenetic regulation","authors":"Nguyen T.B. Nguyen, Sira Gevers, Rutger N.U. Kok, Lotte M. Burgering, Hannah Neikes, Ninouk Akkerman, Max A. Betjes, Marlies C. Ludikhuize, Can Gulersonmez, Edwin C.A. Stigter, Yvonne Vercoulen, Jarno Drost, Hans Clevers, Michiel Vermeulen, Jeroen S. van Zon, Sander J. Tans, Boudewijn M.T. Burgering, Maria J. Rodríguez Colman","doi":"10.1016/j.cmet.2025.01.002","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.002","url":null,"abstract":"Tumors arise from uncontrolled cell proliferation driven by mutations in genes that regulate stem cell renewal and differentiation. Intestinal tumors, however, retain some hierarchical organization, maintaining both cancer stem cells (CSCs) and cancer differentiated cells (CDCs). This heterogeneity, coupled with cellular plasticity enabling CDCs to revert to CSCs, contributes to therapy resistance and relapse. Using genetically encoded fluorescent reporters in human tumor organoids, combined with our machine-learning-based cell tracker, CellPhenTracker, we simultaneously traced cell-type specification, metabolic changes, and reconstructed cell lineage trajectories during tumor organoid development. Our findings reveal distinctive metabolic phenotypes in CSCs and CDCs. We find that lactate regulates tumor dynamics, suppressing CSC differentiation and inducing dedifferentiation into a proliferative CSC state. Mechanistically, lactate increases histone acetylation, epigenetically activating MYC. Given that lactate’s regulation of MYC depends on the bromodomain-containing protein 4 (BRD4), targeting cancer metabolism and BRD4 inhibitors emerge as a promising strategy to prevent tumor relapse.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"47 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143375385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-06DOI: 10.1016/j.cmet.2024.12.011
Thibaux Van der Stede, Alexia Van de Loock, Guillermo Turiel, Camilla Hansen, Andrea Tamariz-Ellemann, Max Ullrich, Eline Lievens, Jan Spaas, Nurten Yigit, Jasper Anckaert, Justine Nuytens, Siegrid De Baere, Ruud Van Thienen, Anneleen Weyns, Laurie De Wilde, Peter Van Eenoo, Siska Croubels, John R. Halliwill, Pieter Mestdagh, Erik A. Richter, Wim Derave
{"title":"Cellular deconstruction of the human skeletal muscle microenvironment identifies an exercise-induced histaminergic crosstalk","authors":"Thibaux Van der Stede, Alexia Van de Loock, Guillermo Turiel, Camilla Hansen, Andrea Tamariz-Ellemann, Max Ullrich, Eline Lievens, Jan Spaas, Nurten Yigit, Jasper Anckaert, Justine Nuytens, Siegrid De Baere, Ruud Van Thienen, Anneleen Weyns, Laurie De Wilde, Peter Van Eenoo, Siska Croubels, John R. Halliwill, Pieter Mestdagh, Erik A. Richter, Wim Derave","doi":"10.1016/j.cmet.2024.12.011","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.12.011","url":null,"abstract":"Plasticity of skeletal muscle is induced by transcriptional and translational events in response to exercise, leading to multiple health and performance benefits. The skeletal muscle microenvironment harbors myofibers and mononuclear cells, but the rich cell diversity has been largely ignored in relation to exercise adaptations. Using our workflow of transcriptome profiling of individual myofibers, we observed that their exercise-induced transcriptional response was surprisingly modest compared with the bulk muscle tissue response. Through the integration of single-cell data, we identified a small mast cell population likely responsible for histamine secretion during exercise and for targeting myeloid and vascular cells rather than myofibers. We demonstrated through histamine H1 or H2 receptor blockade in humans that this paracrine histamine signaling cascade drives muscle glycogen resynthesis and coordinates the transcriptional exercise response. Altogether, our cellular deconstruction of the human skeletal muscle microenvironment uncovers a histamine-driven intercellular communication network steering muscle recovery and adaptation to exercise.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"55 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143192530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-06DOI: 10.1016/j.cmet.2024.12.016
Fabian S. Passini, Bavat Bornstein, Sarah Rubin, Yael Kuperman, Sharon Krief, Evi Masschelein, Tevie Mehlman, Alexander Brandis, Yoseph Addadi, Shira Huri-Ohev Shalom, Erik A. Richter, Tal Yardeni, Amir Tirosh, Katrien De Bock, Elazar Zelzer
{"title":"Piezo2 in sensory neurons regulates systemic and adipose tissue metabolism","authors":"Fabian S. Passini, Bavat Bornstein, Sarah Rubin, Yael Kuperman, Sharon Krief, Evi Masschelein, Tevie Mehlman, Alexander Brandis, Yoseph Addadi, Shira Huri-Ohev Shalom, Erik A. Richter, Tal Yardeni, Amir Tirosh, Katrien De Bock, Elazar Zelzer","doi":"10.1016/j.cmet.2024.12.016","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.12.016","url":null,"abstract":"Systemic metabolism ensures energy homeostasis through inter-organ crosstalk regulating thermogenic adipose tissue. Unlike the well-described inductive role of the sympathetic system, the inhibitory signal ensuring energy preservation remains poorly understood. Here, we show that, via the mechanosensor Piezo2, sensory neurons regulate morphological and physiological properties of brown and beige fat and prevent systemic hypermetabolism. Targeting runt-related transcription factor 3 (Runx3)/parvalbumin (PV) sensory neurons in independent genetic mouse models resulted in a systemic metabolic phenotype characterized by reduced body fat and increased insulin sensitivity and glucose tolerance. Deletion of Piezo2 in PV sensory neurons reproduced the phenotype, protected against high-fat-diet-induced obesity, and caused adipose tissue browning and beiging, likely driven by elevated norepinephrine levels. Finding that brown and beige fat are innervated by Runx3/PV sensory neurons expressing Piezo2 suggests a model in which mechanical signals, sensed by Piezo2 in sensory neurons, protect energy storage and prevent a systemic hypermetabolic phenotype.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"47 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143192532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Interplay between gut microbial communities and metabolites modulates pan-cancer immunotherapy responses","authors":"Xiaoqiang Zhu, Muni Hu, Xiaowen Huang, Lingxi Li, Xiaolin Lin, Xiaoyan Shao, Jiantao Li, Xiaoyue Du, Xinjia Zhang, Rongrong Sun, Tianying Tong, Yanru Ma, Lijun Ning, Yi Jiang, Yue Zhang, Yuqi Shao, Zhenyu Wang, Yilu Zhou, Jinmei Ding, Ying Zhao, Haoyan Chen","doi":"10.1016/j.cmet.2024.12.013","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.12.013","url":null,"abstract":"Immune checkpoint blockade (ICB) therapy has revolutionized cancer treatment but remains effective in only a subset of patients. Emerging evidence suggests that the gut microbiome and its metabolites critically influence ICB efficacy. In this study, we performed a multi-omics analysis of fecal microbiomes and metabolomes from 165 patients undergoing anti-programmed cell death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) therapy, identifying microbial and metabolic entities associated with treatment response. Integration of data from four public metagenomic datasets (<em>n</em> = 568) uncovered cross-cohort microbial and metabolic signatures, validated in an independent cohort (<em>n</em> = 138). An integrated predictive model incorporating these features demonstrated robust performance. Notably, we characterized five response-associated enterotypes, each linked to specific bacterial taxa and metabolites. Among these, the metabolite phenylacetylglutamine (PAGln) was negatively correlated with response and shown to attenuate anti-PD-1 efficacy <em>in vivo</em>. This study sheds light on the interplay among the gut microbiome, the gut metabolome, and immunotherapy response, identifying potential biomarkers to improve treatment outcomes.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"15 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143083542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2025-02-04DOI: 10.1016/j.cmet.2025.01.004
Tingting Zhou, Zhiwei Wang, Xiaowang Lv, Mengting Guo, Ning Zhang, Liangju Liu, Li Geng, Jing Shao, Ka Zhang, Mengru Gao, Aiqin Mao, Yifei Zhu, Fan Yu, Lei Feng, Xiaoyan Wang, Qixiao Zhai, Wei Chen, Xin Ma
{"title":"Targeting gut S. aureofaciens Tü117 serves as a new potential therapeutic intervention for the prevention and treatment of hypertension","authors":"Tingting Zhou, Zhiwei Wang, Xiaowang Lv, Mengting Guo, Ning Zhang, Liangju Liu, Li Geng, Jing Shao, Ka Zhang, Mengru Gao, Aiqin Mao, Yifei Zhu, Fan Yu, Lei Feng, Xiaoyan Wang, Qixiao Zhai, Wei Chen, Xin Ma","doi":"10.1016/j.cmet.2025.01.004","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.004","url":null,"abstract":"Currently, the regulation of specific gut microbial metabolism for the development and/or treatment of hypertension remains largely unexplored. Here, we show that α-lipomycin, produced by <em>Streptomyces aureofaciens</em> (<em>S. aureofaciens</em>) Tü117, is upregulated in the serum of high-salt diet (HSD) mice and patients with essential hypertension. α-lipomycin causes vasodilation impairment involving transient receptor potential vanilloid 4 (TRPV4)-mediated nitric oxide and endothelium-derived hyperpolarizing factor pathways in mice. We also find that <em>Lactobacillus plantarum</em> (<em>L. plantarum</em>) CCFM639 attenuates the increase in blood pressure (BP) potentially through inhibiting the proliferation of <em>S. aureofaciens</em> Tü117 in mice. An exploratory intervention trial indicates that <em>L. plantarum</em> CCFM639 supplementation reduces BPs in subjects newly diagnosed with pre-hypertension or stage 1 hypertension without antihypertensive medication. Our findings provide evidence for a role of <em>S. aureofaciens</em> Tü117-associated α-lipomycin elevation in the pathogenesis of HSD-induced hypertension, highlighting that targeting gut bacteria serves as a new therapeutic intervention for hypertension.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"199 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143084090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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