Science Translational Medicine最新文献

{"title":"Rapid tuberculosis diagnosis from respiratory or blood samples by a low cost, portable lab-in-tube assay","authors":"Brady M. Youngquist,&nbsp;Julian Saliba,&nbsp;Yelim Kim,&nbsp;Thomas J. Cutro,&nbsp;Christopher J. Lyon,&nbsp;Juan Olivo,&nbsp;Ngan Ha,&nbsp;Janelle Fine,&nbsp;Rebecca Colman,&nbsp;Carlos Vergara,&nbsp;James Robinson,&nbsp;Sylvia LaCourse,&nbsp;Richard S. Garfein,&nbsp;Donald G. Catanzaro,&nbsp;Christoph Lange,&nbsp;Eddy Perez-Then,&nbsp;Edward A. Graviss,&nbsp;Charles D. Mitchell,&nbsp;Timothy Rodwell,&nbsp;Bo Ning,&nbsp;Tony Y. Hu","doi":"10.1126/scitranslmed.adp6411","DOIUrl":"10.1126/scitranslmed.adp6411","url":null,"abstract":"<div >Rapid portable assays are needed to improve diagnosis, treatment, and reduce transmission of tuberculosis (TB), but current tests are not suitable for patients in resource-limited settings with high TB burden. Here we report a low complexity, lab-in-tube system that is read by an integrated handheld device that detects <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) DNA in blood and respiratory samples from a variety of clinical settings. This microprocessor-controlled device uses an LCD user interface to control assay performance, automate assay analysis, and provide results in a simple readout. This point-of-care single-tube assay uses a DNA enrichment membrane and a low-cost cellulose disc containing lyophilized recombinase polymerase amplification and CRISPR-Cas12a reagents to attain single-nucleotide specificity and high sensitivity within 1 hour of sample application, without a conventional DNA isolation procedure. Assay results obtained with serum cell–free DNA isolated from a cohort of children aged 1 to 16 years detected pulmonary and extrapulmonary TB with high sensitivity versus culture and GeneXpert MTB/RIF results (81% versus 55% and 68%) and good specificity (94%), meeting the World Health Organization target product profile criteria for new nonsputum TB diagnostics. Changes in assay results for serum isolated during treatment were also highly predictive of clinical response. Results obtained with noninvasive sputum and saliva specimens from adults with bacteriologically confirmed pulmonary TB were also comparable to those reported for reference methods. This rapid and inexpensive lab-in-tube assay approach thus represents one means to address the need for point-of-care TB diagnostics useable in low-resource settings.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143806090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mRNA export pathway licenses viral mimicry response and antitumor immunity by actively exporting nuclear retroelement transcripts","authors":"Xiaoqiang Wang,&nbsp;Jiaxing Jin,&nbsp;Han Yan,&nbsp;Jinhua Liu,&nbsp;Shan Huang,&nbsp;Hui Bai,&nbsp;Mingrui Guo,&nbsp;Xinyue Cheng,&nbsp;Ting Deng,&nbsp;Yi Ba,&nbsp;Yong Gu,&nbsp;Xin Gao,&nbsp;Deqing Hu","doi":"10.1126/scitranslmed.ado4370","DOIUrl":"10.1126/scitranslmed.ado4370","url":null,"abstract":"<div >Nuclear retroelement transcripts (RTs), which can be elicited both transcriptionally and posttranscriptionally, form double-stranded RNA (dsRNA) in cytosol to trigger the viral mimicry response (VMR) and antitumor immunity. However, the strength of the induced VMR varies tremendously across tumor types, and the underlying mechanisms remain poorly understood. Here, we demonstrate that the mRNA export pathway modulates the VMR through actively exporting nuclear RTs for cytosolic dsRNA formation after their induction. Tumor cells hijack this process for immune evasion through aberrant coactivator-associated arginine methyltransferase 1 (CARM1) expression. Mechanistically, we show that the cytoplasmic transportation of RTs by the mRNA export pathway is counteracted by the RNA exosome, which cleaves multiple transcripts within this pathway, including those encoding the essential DExD-box helicase 39A (DDX39A) and the adaptor protein ALYREF. CARM1 enhances the RNA exosome activity to attenuate the nuclear export of RTs by the mRNA export pathway through two synergistic mechanisms: (i) transcriptionally activating several RNA exosome components and (ii) posttranslationally methylating arginine 6 of the RNA exosome subunit EXOSC1, which protects it from proteasome-mediated degradation. Collectively, our study highlights the critical active regulatory role of the mRNA export pathway in transporting nuclear RTs into the cytosol for triggering the VMR and tumor immunity. Furthermore, we propose that enhancing the mRNA export pathway activity, either through CARM1 inhibition or RNA exosome modulation, could reinforce the therapeutic agent-induced VMR, thus holding the promise for overcoming tumor immune evasion and immunotherapy resistance.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/scitranslmed.ado4370","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143806170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Succinate-loaded tumor cell–derived microparticles reprogram tumor-associated macrophage metabolism","authors":"Shuya Lu,&nbsp;Jiexiao Li,&nbsp;Yonggang Li,&nbsp;Shichuan Liu,&nbsp;Yutong Liu,&nbsp;Yue Liang,&nbsp;Xifen Zheng,&nbsp;Yiyang Chen,&nbsp;Jinghui Deng,&nbsp;Huafeng Zhang,&nbsp;Jingwei Ma,&nbsp;Jiadi Lv,&nbsp;Yugang Wang,&nbsp;Bo Huang,&nbsp;Ke Tang","doi":"10.1126/scitranslmed.adr4458","DOIUrl":"10.1126/scitranslmed.adr4458","url":null,"abstract":"<div >The tumor microenvironment predominantly polarizes tumor-associated macrophages (TAMs) toward an M2-like phenotype, thereby inhibiting antitumor immune responses. This process is substantially affected by metabolic reprogramming; however, reeducating TAMs to enhance their antitumor capabilities through metabolic remodeling remains a challenge. Here, we show that tumor-derived microparticles loaded with succinate (SMPs) can remodel the metabolic state of TAMs. SMPs promote classical M1-like polarization of macrophages by enhancing glycolysis and attenuating the tricarboxylic acid (TCA) cycle in a protein succinylation–dependent manner. Mechanistically, succinate is delivered into the mitochondria and nucleus by SMPs, leading to succinylation of isocitrate dehydrogenase 2 (IDH2) and histone H3K122 within the lactate dehydrogenase A (<i>Ldha</i>) promoter region. Our findings provide a distinct approach for TAM polarization using cell membrane–derived microparticles loaded with endogenous metabolites, a platform that may be used more broadly for posttranslational modification–based tumor immunotherapy.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143806086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The response to anti–PD-1 and anti–LAG-3 checkpoint blockade is associated with regulatory T cell reprogramming","authors":"Annah S. Rolig,&nbsp;Xiyu Peng,&nbsp;Elizabeth R. Sturgill,&nbsp;Nisha Holay,&nbsp;Melissa Kasiewicz,&nbsp;Courtney Mick,&nbsp;Grace Helen Mcgee,&nbsp;William Miller,&nbsp;Yoshinobu Koguchi,&nbsp;Johanna Kaufmann,&nbsp;Niranjan Yanamandra,&nbsp;Sue Griffin,&nbsp;James Smothers,&nbsp;Matthew Adamow,&nbsp;Jasme Lee,&nbsp;Ronglai Shen,&nbsp;Margaret K. Callahan,&nbsp;William L. Redmond","doi":"10.1126/scitranslmed.adk3702","DOIUrl":"10.1126/scitranslmed.adk3702","url":null,"abstract":"<div >Immune checkpoint blockade (ICB) has revolutionized cancer treatment; however, many patients develop therapeutic resistance. We previously identified and validated a pretreatment peripheral blood biomarker, characterized by a high frequency of LAG-3⁺ lymphocytes, that predicts resistance in patients receiving anti–PD-1 (aPD-1) ICB. To better understand the mechanism of aPD-1 resistance, we identified murine tumor models with a high LAG-3⁺ lymphocyte frequency (LAG-3^hi), which were resistant to aPD-1 therapy, and LAG-3^lo murine tumor models that were aPD-1 sensitive, recapitulating the predictive biomarker we previously described in patients. LAG-3^hi tumor-bearing mice were sensitive to aPD-1 + anti–LAG-3 (aLAG-3) therapy, and this benefit was CD8⁺ T cell dependent. The efficacy of combination therapy was enhanced in LAG-3^hi (but not LAG-3^lo) mice with depletion of CD4⁺ T cells. Furthermore, responses to aPD-1 + aLAG-3 correlated with regulatory T cell (T_reg) phenotypic plasticity in LAG-3^hi mice, suggesting a specific role for T_regs in response to aPD-1 + aLAG-3 treatment. Using T_reg fate–tracking <i>Foxp3^GFP-Cre-ERT2</i> × ROSA^YFP reporter mice, we demonstrated that expanded populations of unstable T_regs correlated with improved response to combination therapy in LAG-3^hi mice. Complementing these preclinical data, an increased proportion of unstable T_regs also correlated with higher response rate and improved survival after aPD-1 + aLAG-3 therapy in a cohort of patients with metastatic melanoma (<i>n</i> = 117). These data indicate that T_reg phenotypic plasticity affects aPD-1 + aLAG-3 responsiveness, which may represent a biomarker to aid patient selection and a rational therapeutic target for a subset of PD-1–refractory patients.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143806089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial genomics: Mapping the landscape of fibrosis","authors":"Prasad Palani Velu,&nbsp;Roxanna E. Abhari,&nbsp;Neil C. Henderson","doi":"10.1126/scitranslmed.adm6783","DOIUrl":"10.1126/scitranslmed.adm6783","url":null,"abstract":"<div >Organ fibrosis causes major morbidity and mortality worldwide. Treatments for fibrosis are limited, with organ transplantation being the only cure. Here, we review how various state-of-the-art spatial genomics approaches are being deployed to interrogate fibrosis across multiple organs, providing exciting insights into fibrotic disease pathogenesis. These include the detailed topographical annotation of pathogenic cell populations and states, detection of transcriptomic perturbations in morphologically normal tissue, characterization of fibrotic and homeostatic niches and their cellular constituents, and in situ interrogation of ligand-receptor interactions within these microenvironments. Together, these powerful readouts enable detailed analysis of fibrosis evolution across time and space.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143806091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum for the Research Article “A gut Eggerthella lenta–derived metabolite impairs neutrophil function to aggravate bacterial lung infection” by L.-L. Wang et al.","authors":"","doi":"10.1126/scitranslmed.adx6062","DOIUrl":"10.1126/scitranslmed.adx6062","url":null,"abstract":"","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143809977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collagen V regulates renal function after kidney injury and can be pharmacologically targeted to enhance kidney repair in mice","authors":"Lianjiu Su,&nbsp;Qihao Sun,&nbsp;Yusheng Li,&nbsp;Juan Felipe Alvarez,&nbsp;Bo Tao,&nbsp;Guanglin Zhang,&nbsp;Yiqian Gu,&nbsp;Mark R. Hanudel,&nbsp;Alejandro Espinoza,&nbsp;Linlin Zhang,&nbsp;Calvin Pan,&nbsp;James R. Hilser,&nbsp;Jaana A. Hartiala,&nbsp;Shen Li,&nbsp;Matteo Pellegrini,&nbsp;Hooman Allayee,&nbsp;Aldons J. Lusis,&nbsp;Arjun Deb","doi":"10.1126/scitranslmed.ads7714","DOIUrl":"10.1126/scitranslmed.ads7714","url":null,"abstract":"<div >Kidney fibrosis determines clinical outcomes in individuals with chronic kidney disease (CKD). The stoichiometric ratio of collagens in renal scar differs from that of healthy kidney extracellular matrix (ECM), but the functional importance of altered collagen types in injured kidneys remains unclear. Using human population studies, we show that circulating protein and renal mRNA amounts of collagen V A1 (COL5A1) exhibited associations with kidney disease and incident CKD risk. We show that <i>Col5a1</i> regulates the degree of postinjury fibrosis and renal function. Mice with conditionally knocked out <i>Col5a1</i> (<i>Col5a1</i> CKO) exhibited decreased renal function and greater renal fibrosis after dietary adenine- or ureteric obstruction–mediated kidney injury. Renal fibroblasts in <i>Col5a1</i> CKO animals up-regulated the profibrotic αvβ3 integrin. Inhibition of αvβ3 signaling with a small molecule, cilengitide, rescued postinjury renal function in <i>Col5a1</i> CKO animals. Using the hybrid mouse diversity panel that comprises 100 diverse inbred strains of mice, we observed that gene expression of <i>Col5a1</i> after injury exhibited genetic variation across 100 strains. Strains with low <i>Col5a1</i> expression after injury exhibited worse renal function compared with animals that had higher degrees of expression. We next measured <i>Col5a1</i> expression in peripheral blood mononuclear cells in mice to identify nonresponder strains that did not have increased <i>Col5a1</i> expression after kidney injury. We observed that administration of cilengitide in nonresponder strains significantly rescued postinjury renal fibrosis and function. These studies point to the feasibility of precision medicine approaches to target <i>Col5a1</i> for enhancing renal repair.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 793","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143806168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oligodendroglial precursor cells modulate immune response and early demyelination in a murine model of multiple sclerosis","authors":"Qi Wang,&nbsp;Taida Huang,&nbsp;Zihan Zheng,&nbsp;Yixun Su,&nbsp;Zhonghao Wu,&nbsp;Cong Zeng,&nbsp;Guangdan Yu,&nbsp;Yang Liu,&nbsp;Xiaorui Wang,&nbsp;Hui Li,&nbsp;Xiaoying Chen,&nbsp;Zhuoxu Jiang,&nbsp;Jinyu Zhang,&nbsp;Yuan Zhuang,&nbsp;Yi Tian,&nbsp;Qingwu Yang,&nbsp;Alexei Verkhratsky,&nbsp;Ying Wan,&nbsp;Chenju Yi,&nbsp;Jianqin Niu","doi":"10.1126/scitranslmed.adn9980","DOIUrl":"10.1126/scitranslmed.adn9980","url":null,"abstract":"<div >Reproducing the pathophysiology of human multiple sclerosis (MS) in animal models is critical to identifying mechanisms triggering demyelination and to developing early intervention strategies. Here, we aimed to model overactivated Wnt (wingless-related integration site) signaling previously shown in postmortem brain tissues of patients with MS by inducing experimental autoimmune encephalomyelitis (EAE) in <i>Pdgfra^CreER;Apc^fl/fl</i> and <i>Olig2^Cre;Apc^fl/fl</i> mice. These mice have overactivated Wnt signaling in oligodendrocyte precursor cells (OPCs) because of a conditional knockout of the pathway repressor adenomatous polyposis coli (APC). <i>Pdgfra^CreER;Apc^fl/fl</i> EAE mice exhibited increased expression of markers for Wnt activation such as Axis inhibition protein 2 (AXIN2) and Wnt inhibitory factor 1 (WIF1) in OPCs and showed exacerbated EAE progression in both the spinal cord and the brain. Genetic or antibody-mediated ablation of CC-chemokine ligand 4 (CCL4) prevented infiltration of CD4⁺ T cells and arrested disease progression in these mice. A characterization of CNS (central nervous system) immune cell clusters identified an augmented subpopulation of NK1.1⁺CD11b⁺Gr-1⁺ cytotoxic macrophages in <i>Pdgfra^CreER;Apc^fl/fl</i> EAE mice. Microinjection of this subpopulation of macrophages into the brains of wild-type C57/B6J mice was sufficient to induce demyelination. Ablation of CD4⁺ T cells prevented the effects of Wnt overactivation on demyelination and immune cell infiltration. Antagonizing chemokine receptor 5 (CCR5) using a European Medicines Agency–approved drug, maraviroc, reduced immune cell infiltration, alleviated demyelination, and attenuated EAE progression. We found an OPC-orchestrated immune cellular network that instigates early demyelination, provides insight into MS pathophysiology, and suggests avenues for early interventions.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 792","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human iPSC–derived nephron progenitor cells treat acute kidney injury and chronic kidney disease in mouse models","authors":"Toshikazu Araoka,&nbsp;Kosuke Toyohara,&nbsp;Makoto Ryosaka,&nbsp;Chihiro Inui,&nbsp;Maasa Matsuura,&nbsp;Chen Ma,&nbsp;Jun Watahiki,&nbsp;Zhongwei Li,&nbsp;Mio Iwasaki,&nbsp;Akira Watanabe,&nbsp;Ryuji Yokokawa,&nbsp;Yasuhiko Tabata,&nbsp;Juan Carlos Izpisua Belmonte,&nbsp;Kenji Osafune","doi":"10.1126/scitranslmed.adt5553","DOIUrl":"10.1126/scitranslmed.adt5553","url":null,"abstract":"<div >The number of patients requiring dialysis therapy continues to increase worldwide because of the lack of effective treatments for chronic kidney disease (CKD). Furthermore, no curative treatments for acute kidney injury (AKI) have been established. The therapeutic effects of human induced pluripotent stem cell–derived nephron progenitor cells (hiPSC-NPCs) on AKI have been reported in mice but not clinically confirmed. There are also no reports examining the therapeutic potential of hiPSC-NPCs on CKD. Although large numbers of uniform hiPSC-NPCs are required for cell therapies for AKI and CKD, effective expansion cultures remain to be developed. Here, we established a culture medium for cells that enabled more than 100-fold proliferation of hiPSC-NPCs from multiple hiPSC lines in two passages. We demonstrated that hiPSC-NPCs expanded by our medium named CFY or by their conditioned medium alone attenuated kidney injury and improved survival in cisplatin-induced AKI mice. We also observed that hiPSC-NPCs prevented kidney functional decline, interstitial fibrosis, and senescence in aristolochic acid–induced CKD mice. In addition, we found c-MET to be a specific cell surface marker for hiPSC-NPCs and confirmed that purified c-MET⁺ hiPSC-NPCs had therapeutic effects on AKI and CKD mice. Furthermore, we found that hiPSC-NPCs exerted their therapeutic effects in AKI and CKD mice by secreting vascular endothelial growth factor A. Expanded hiPSC-NPCs may be useful cell therapies for AKI and CKD and may open avenues for treating kidney diseases.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 792","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Path to a cure for debilitating pregnancy sickness","authors":"Marlena Fejzo","doi":"10.1126/scitranslmed.adw9351","DOIUrl":"10.1126/scitranslmed.adw9351","url":null,"abstract":"<div >Identification of GDF15 as a cause of severe nausea and vomiting during pregnancy is opening new doors for treatment and prevention.</div>","PeriodicalId":21580,"journal":{"name":"Science Translational Medicine","volume":"17 792","pages":""},"PeriodicalIF":15.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}