Cell metabolismPub Date : 2025-09-16DOI: 10.1016/j.cmet.2025.08.008
Christina Mayerhofer, Dan Li, Trine Kristiansen, Ernst Mayerhofer, Azeem Sharda, Giulia Schiroli, Karin Gustafsson, Lingli He, Michael Mazzola, Sam Keyes, Anna Kiem, Eve Crompton, Yanxin Xu, Sovannarith Korm, Zhixun Dou, Charles Vidoudez, Peter G. Miller, Nick van Gastel, Timothy A. Graubert, David T. Scadden
{"title":"OGFOD1 enables AML chemo- and nutrient stress resistance by regulating protein synthesis","authors":"Christina Mayerhofer, Dan Li, Trine Kristiansen, Ernst Mayerhofer, Azeem Sharda, Giulia Schiroli, Karin Gustafsson, Lingli He, Michael Mazzola, Sam Keyes, Anna Kiem, Eve Crompton, Yanxin Xu, Sovannarith Korm, Zhixun Dou, Charles Vidoudez, Peter G. Miller, Nick van Gastel, Timothy A. Graubert, David T. Scadden","doi":"10.1016/j.cmet.2025.08.008","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.008","url":null,"abstract":"Acute myeloid leukemia (AML) commonly relapses after initial chemotherapy response. We assessed metabolic adaptations in chemoresistant cells <em>in vivo</em> before overt relapse, identifying altered branched-chain amino acid (BCAA) levels in patient-derived xenografts (PDXs) and immunophenotypically identified leukemia stem cells from AML patients. Notably, this was associated with increased BCAA transporter expression with low BCAA catabolism. Restricting BCAAs further reduced chemoresistant AML cells, but relapse still occurred. Among the persisting cells, we found an unexpected increase in protein production. This was accompanied by elevated translation of 2-oxoglutarate- and iron-dependent oxygenase 1 (OGFOD1), a known ribosomal dioxygenase that adjusts the fidelity of tRNA anticodon pairing with coding mRNA. We found that OGFOD1 upregulates protein synthesis in AML, driving disease aggressiveness. Inhibiting OGFOD1 impaired translation processing, decreased protein synthesis and improved animal survival even with chemoresistant AML while sparing normal hematopoiesis. Leukemic cells can therefore persist despite the stress of chemotherapy and nutrient deprivation through adaptive control of translation. Targeting OGFOD1 may offer a distinctive, translation-modifying means of reducing the chemopersisting cells that drive relapse.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"15 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145067875","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 : 2025-09-05DOI: 10.1016/j.cmet.2025.08.005
Vitor Rosetto Muñoz, Francois Moreau, Marion Soto, Yoshiyuki Watanabe, Loc-Duyen Pham, Jimmy Zhong, Sam Zimmerman, Bruna B. Brandao, Khyati Girdhar, Julian Avila, Hui Pan, Jonathan M. Dreyfuss, Michael Y. Mi, Robert E. Gerszten, Emrah Altindis, Aleksandar Kostic, Clary B. Clish, C. Ronald Kahn
{"title":"Portal vein-enriched metabolites as intermediate regulators of the gut microbiome in insulin resistance","authors":"Vitor Rosetto Muñoz, Francois Moreau, Marion Soto, Yoshiyuki Watanabe, Loc-Duyen Pham, Jimmy Zhong, Sam Zimmerman, Bruna B. Brandao, Khyati Girdhar, Julian Avila, Hui Pan, Jonathan M. Dreyfuss, Michael Y. Mi, Robert E. Gerszten, Emrah Altindis, Aleksandar Kostic, Clary B. Clish, C. Ronald Kahn","doi":"10.1016/j.cmet.2025.08.005","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.005","url":null,"abstract":"Diet and obesity contribute to insulin resistance and type 2 diabetes, in part via the gut microbiome. To explore the role of gut-derived metabolites in this process, we assessed portal/peripheral blood metabolites in mice with different risks of obesity/diabetes, challenged with a high-fat diet (HFD) + antibiotics. In diabetes/obesity-prone C57BL/6J mice, 111 metabolites were portally enriched and 74 were peripherally enriched, many of which differed in metabolic-syndrome-resistant 129S1/129S6 mice. Vancomycin treatment of HFD-fed C57BL/6J mice modified the microbiome and the portal/peripheral ratio of many metabolites, including upregulating tricarboxylic acid (TCA) cycle-related metabolites, like mesaconate, in portal blood. Treatment of isolated hepatocytes with mesaconate, itaconate, or citraconate improved insulin signaling and transcriptionally regulated genes involved in gluconeogenesis, fatty acid oxidation, and lipogenesis <em>in vitro</em> and <em>in vivo</em>. In humans, citraconate levels are inversely correlated with plasma glucose. Thus, portal versus peripheral metabolites play important roles in mediating effects of the microbiome on hepatic metabolism and the pathogenesis of HFD-related insulin resistance.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"35 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144996037","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 : 2025-09-04DOI: 10.1016/j.cmet.2025.08.002
Yuqing Zhang, Zi-Jiang Chen, Han Zhao
{"title":"Polycystic ovary syndrome: A metabolic disorder with therapeutic opportunities","authors":"Yuqing Zhang, Zi-Jiang Chen, Han Zhao","doi":"10.1016/j.cmet.2025.08.002","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.002","url":null,"abstract":"Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine disorder characterized by intertwined reproductive and metabolic abnormalities. While its causal origins remain incompletely understood, accumulating evidence suggests metabolic dysfunctions—manifested by insulin resistance, obesity, hyperglycemia, and dyslipidemia—as key contributors to the pathogenesis and progression of PCOS. Emerging interventions targeting these metabolic disturbances, including caloric restriction, GLP-1-based therapies, and bariatric surgery, have shown efficacy in alleviating PCOS symptoms and potentially blocking their inheritance. By addressing the metabolic roots and therapeutic opportunities in PCOS, this perspective highlights a critical shift in fundamentally recognizing PCOS as a metabolic disorder. The future promises more metabolic-focused research to unravel the underlying pathogenesis and develop precise, long-term strategies for managing this complex disease.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"29 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144987598","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":"Mitochondrial dysfunction reveals H2S-mediated synaptic sulfhydration as a potential mechanism for autism-associated social defects","authors":"Panpan Xian, Mengmeng Wang, Rougang Xie, Hongyu Ma, Weian Zheng, Junjun Kang, Yujiang Chen, Hanze Liu, Songqi Dong, Haiying Liu, Wenle Zhang, Honghui Mao, Fang Wang, Ning Yang, Jun Yu, Ningxia Zhao, Yazhou Wang, Shengxi Wu","doi":"10.1016/j.cmet.2025.08.003","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.003","url":null,"abstract":"Clinical studies have identified multiple mitochondrial disturbances in the peripheral tissues of patients with autism. However, how neuronal metabolism contributes to the autism-associated phenotype remains unclear. In this study, we focused on the anterior cingulate cortex (ACC) and reported hydrogen sulfide (H<sub>2</sub>S) elevation as a common outcome to mitochondrial dysfunction in <em>Shank3b</em><sup>−/−</sup> and <em>Fmr1</em><sup><em>−/y</em></sup> neurons. Cystathionine β-synthase overexpression in ACC impaired synaptic transmission and social function in wild-type mice, while its knockdown effectively rescued synaptic and social defects in both autism mouse models. Dramatic changes in synaptic protein sulfhydration were observed in <em>Shank3b</em><sup>−/−</sup> ACC, with over-sulfhydration of mGluR5 validated in both models. Ablating mGluR5 sulfhydration partially alleviated social deficits in both strains. Furthermore, sulfur amino acid restriction ameliorated social dysfunction in <em>Shank3b</em><sup>−/−</sup> and <em>Fmr1</em><sup><em>−/y</em></sup> mice and synaptic defects in corresponding human neurons. Our data indicate that excessive H<sub>2</sub>S and synaptic protein sulfhydration may serve as potential mechanisms underlying the autism-associated social dysfunction.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"29 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144930484","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 : 2025-09-02DOI: 10.1016/j.cmet.2025.06.012
Chi Kin Wong, Bernardo Yusta, Jason C.L. Tong, Johannes Broichhagen, David J. Hodson, Daniel J. Drucker
{"title":"Reassessment of antibody-based detection of the murine T cell GLP-1 receptor","authors":"Chi Kin Wong, Bernardo Yusta, Jason C.L. Tong, Johannes Broichhagen, David J. Hodson, Daniel J. Drucker","doi":"10.1016/j.cmet.2025.06.012","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.06.012","url":null,"abstract":"Glucagon-like peptide 1 receptor (GLP-1R) agonists exhibit anti-inflammatory actions, yet the importance of direct immune cell GLP-1R signaling remains uncertain. Although T cells respond to GLP-1, low receptor abundance and suboptimal antisera complicate efforts to characterize immune cell GLP-1R signaling. Here, we evaluate three frequently utilized GLP-1R antibodies, revealing that one of several antibodies, AGR-021, lack ideal specificity for detecting the GLP-1R in mice. Immunostaining with AGR-021 using tissues from two independent GLP-1R knockout mouse lines reveals persistent immunoreactive signals in GLP-1R-null pancreatic islets. Similarly, flow cytometry using AGR-021 reveals no reduction in AGR-021 immunoreactivity in GLP-1R-null splenic T cells. Moreover, western blotting detects AGR-021-immunoreactive proteins from a GLP-1R-negative cell line and fails to detect immunoreactive GLP-1R of the correct size upon overexpression of the receptor. Our findings reveal caveats governing use of multiple widely used GLP-1R antibodies, reemphasizing the importance of rigorous antibody validation for inferring accurate GLP-1R expression.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"42 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928466","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 : 2025-08-28DOI: 10.1016/j.cmet.2025.08.004
Jessica M. Preston, Jo Iversen, Antonia Hufnagel, Line Hjort, Jodie Taylor, Clara Sanchez, Victoria George, Ann N. Hansen, Lars Ängquist, Susan Hermann, Jeffrey M. Craig, Signe Torekov, Christian Lindh, Karin S. Hougaard, Marcelo A. Nóbrega, Stephen J. Simpson, Romain Barrès
{"title":"Effect of ultra-processed food consumption on male reproductive and metabolic health","authors":"Jessica M. Preston, Jo Iversen, Antonia Hufnagel, Line Hjort, Jodie Taylor, Clara Sanchez, Victoria George, Ann N. Hansen, Lars Ängquist, Susan Hermann, Jeffrey M. Craig, Signe Torekov, Christian Lindh, Karin S. Hougaard, Marcelo A. Nóbrega, Stephen J. Simpson, Romain Barrès","doi":"10.1016/j.cmet.2025.08.004","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.004","url":null,"abstract":"Consumption of ultra-processed food is associated with increased caloric intake and impaired health. Here, we conducted a nutrition trial (NCT05368194) with controlled, 2 × 2 crossover design and tested whether ultra-processed food impairs reproductive and metabolic fitness, with further aggravation by excess caloric intake. Comparing the response from an unprocessed to ultra-processed diet identified increased body weight and low-density lipoprotein (LDL):high-density lipoprotein (HDL) ratio, independent of caloric load. Several hormones involved in energy metabolism and spermatogenesis were affected, including decreased levels of growth/differentiation factor 15 and follicle-stimulating hormone. Sperm quality trended toward impairment, with a decrease in total motility. Differential accumulation of pollutants between the discordant diets were detected, such as decreased plasma lithium and a trend for increased levels of the phthalate mono(4-methyl-7-carboxyheptyl)phthalate (cxMINP) in serum, following the ultra-processed diet. Alteration in caloric load alone had distinct effects on the measured outcomes. This study provides evidence that consumption of ultra-processed food is detrimental for cardiometabolic and reproductive outcomes, regardless of excessive caloric intake.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"28 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144911214","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 : 2025-08-27DOI: 10.1016/j.cmet.2025.08.001
Moubin Lin, Juan Wang, Yongshuai Chai, Xin Chen, Danyang Zhao, Zhangdan Xie, Jiebang Jiang, Hong Li, Li Huang, Siwei Xing, Dashi Qi, Xinyu Mei
{"title":"Homocysitaconate controls inflammation through reshaping methionine metabolism and N-homocysteinylation","authors":"Moubin Lin, Juan Wang, Yongshuai Chai, Xin Chen, Danyang Zhao, Zhangdan Xie, Jiebang Jiang, Hong Li, Li Huang, Siwei Xing, Dashi Qi, Xinyu Mei","doi":"10.1016/j.cmet.2025.08.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.001","url":null,"abstract":"Inflammation and its metabolic-network interactions generate novel regulatory molecules with translational implications. Here, we identify the immunometabolic crosstalk that generates homocysitaconate, a metabolite formed by homocysteine and itaconate adduction catalyzed by S-adenosyl-L-homocysteine hydrolase (AHCY). Homocysitaconate increases 152-fold during inflammation and exhibits anti-inflammatory effects. Mechanistically, homocysitaconate binds to the D312 residue of the pro-inflammatory protein methionyl-tRNA synthetase (MARS), inhibiting its function and reshaping methionine metabolism to feedback-brake the early activation of the N-homocysteinylation pathway. This metabolic switch facilitates NLR family pyrin domain-containing 3 (NLRP3) ubiquitination to control inflammation. Homocysitaconate demonstrates therapeutic effects in sepsis, high-fat-diet-induced inflammation, and colitis models. Boosting endogenous homocysitaconate synthesis through nicotinamide adenine dinucleotide (NAD<sup>+</sup>)-dependent AHCY activation (using nicotinamide riboside and pyruvate) also inhibits inflammation by targeting the MARS/NLRP3-N-homocysteinylation cascade. This study establishes homocysitaconate as an anti-inflammatory metabolite that serves as a homeostatic governor by reprogramming protein modification switches, introducing both metabolic timing regulation and clinical strategies to manage inflammatory complications.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"24 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906071","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 : 2025-08-25DOI: 10.1016/j.cmet.2025.07.010
Dishu Zhou, Ying Chen, Panpan Liu, Kun Zhu, Juliet Holder-Haynes, S. Julie-Ann Lloyd, Cam Mong La, Inna I. Astapova, Seunghee Choa, Ying Xiong, Hosung Bae, Marlene Aguilar, Hongyuan Yang, Yu A. An, Zheng Sun, Mark A. Herman, Xia Gao, Liming Pei, Cholsoon Jang, Joshua D. Rabinowitz, Dongyin Guan
{"title":"Genetics-nutrition interactions control diurnal enhancer-promoter dynamics and liver lipid metabolism","authors":"Dishu Zhou, Ying Chen, Panpan Liu, Kun Zhu, Juliet Holder-Haynes, S. Julie-Ann Lloyd, Cam Mong La, Inna I. Astapova, Seunghee Choa, Ying Xiong, Hosung Bae, Marlene Aguilar, Hongyuan Yang, Yu A. An, Zheng Sun, Mark A. Herman, Xia Gao, Liming Pei, Cholsoon Jang, Joshua D. Rabinowitz, Dongyin Guan","doi":"10.1016/j.cmet.2025.07.010","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.07.010","url":null,"abstract":"The circadian clock controls 24-h rhythmic processes. However, how genetic variations outside clock genes impact peripheral diurnal rhythms remains largely unknown. Here, we find that genetic variation contributes to different diurnal patterns of hepatic gene expression in both humans and mice. Nutritional challenges alter the rhythmicity of gene expression in mouse liver in a strain-specific manner. Remarkably, genetics and nutrition interdependently control more than 80% of rhythmic gene and enhancer-promoter interactions (E-PIs), with a noncanonical clock regulator, estrogen-related receptor gamma (ESRRγ), emerging as a top transcription factor during motif mining. Knockout of <em>Esrrγ</em> abolishes strain-specific metabolic processes in response to diet in mice, while single-nucleotide polymorphisms (SNPs) associated with rhythmic gene expression are enriched in E-PIs in steatotic human livers and correlate with lipid metabolism traits. These findings reveal a previously underappreciated temporal aspect of genetics-environment interaction in regulating lipid metabolic traits, with implications for individual variations in obesity-associated disease susceptibility and personalized chronotherapy.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"15 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900555","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 : 2025-08-13DOI: 10.1016/j.cmet.2025.07.009
Robert Hansford, Sophie Buller, Anthony H. Tsang, Simon Benoit, Anna G. Roberts, Emmy Erskine, Thomas Brown, Valentina Pirro, Frank Reimann, Norio Harada, Nobuya Inagaki, Ricardo J. Samms, Johannes Broichhagen, David J. Hodson, Alice Adriaenssens, Soyoung Park, Clemence Blouet
{"title":"Glucose-dependent insulinotropic polypeptide receptor signaling in oligodendrocytes increases the weight-loss action of GLP-1R agonism","authors":"Robert Hansford, Sophie Buller, Anthony H. Tsang, Simon Benoit, Anna G. Roberts, Emmy Erskine, Thomas Brown, Valentina Pirro, Frank Reimann, Norio Harada, Nobuya Inagaki, Ricardo J. Samms, Johannes Broichhagen, David J. Hodson, Alice Adriaenssens, Soyoung Park, Clemence Blouet","doi":"10.1016/j.cmet.2025.07.009","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.07.009","url":null,"abstract":"The next generation of obesity medicines harness the activity of the glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1 receptors (GIPR and GLP-1R), but their mechanism of action remains unclear. Here, we report that the GIPR is enriched in oligodendrocytes and GIPR signaling bidirectionally regulates oligodendrogenesis. In mice with adult-onset deletion of GIPR in oligodendrocytes, GIPR agonism fails to enhance the weight-loss effects of GLP-1R agonism. Mechanistically, GIPR agonism increases brain access of GLP-1R agonists, and GIPR signaling in oligodendrocytes is required for this effect. In addition, we show that vasopressin neurons of the paraventricular hypothalamus are necessary for the weight-loss response to GLP-1R activation, targeted by peripherally administered GLP-1R agonists via their axonal compartment, and this access is increased by activation of the GIPR in oligodendrocytes. Collectively, our findings identify a novel mechanism by which incretin therapies may function to promote synergistic weight loss in the management of excess adiposity.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"53 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144825263","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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