Nadine Tuechler, Mira Lea Burtscher, Martin Garrido-Rodriguez, Muzamil Majid Khan, Dénes Türei, Christian Tischer, Sarah Kaspar, Jennifer Jasmin Schwarz, Frank Stein, Mandy Rettel, Rafael Kramann, Mikhail M Savitski, Julio Saez-Rodriguez, Rainer Pepperkok
{"title":"Dynamic multi-omics and mechanistic modeling approach uncovers novel mechanisms of kidney fibrosis progression.","authors":"Nadine Tuechler, Mira Lea Burtscher, Martin Garrido-Rodriguez, Muzamil Majid Khan, Dénes Türei, Christian Tischer, Sarah Kaspar, Jennifer Jasmin Schwarz, Frank Stein, Mandy Rettel, Rafael Kramann, Mikhail M Savitski, Julio Saez-Rodriguez, Rainer Pepperkok","doi":"10.1038/s44320-025-00116-2","DOIUrl":"https://doi.org/10.1038/s44320-025-00116-2","url":null,"abstract":"<p><p>Kidney fibrosis, characterized by excessive extracellular matrix deposition, is a progressive disease that, despite affecting 10% of the population, lacks specific treatments and suitable biomarkers. This study presents a comprehensive, time-resolved multi-omics analysis of kidney fibrosis using an in vitro model system based on human kidney PDGFRβ<sup>+</sup> mesenchymal cells aimed at unraveling disease mechanisms. Using transcriptomics, proteomics, phosphoproteomics, and secretomics, we quantified over 14,000 biomolecules across seven time points following TGF-β stimulation. This revealed distinct temporal patterns in the expression and activity of known and potential kidney fibrosis markers and modulators. Data integration resulted in time-resolved multi-omic network models which allowed us to propose mechanisms related to fibrosis progression through early transcriptional reprogramming. Using siRNA knockdowns and phenotypic assays, we validated predictions and regulatory mechanisms underlying kidney fibrosis. In particular, we show that several early-activated transcription factors, including FLI1 and E2F1, act as negative regulators of collagen deposition and propose underlying molecular mechanisms. This work advances our understanding of the pathogenesis of kidney fibrosis and provides a resource to be further leveraged by the community.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":""},"PeriodicalIF":8.5,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234581","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":"Spatial proteomics in translational and clinical research.","authors":"Peter Horvath, Fabian Coscia","doi":"10.1038/s44320-025-00101-9","DOIUrl":"10.1038/s44320-025-00101-9","url":null,"abstract":"","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"526-530"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ulrich Goldmann, Tabea Wiedmer, Andrea Garofoli, Vitaly Sedlyarov, Manuel Bichler, Ben Haladik, Gernot Wolf, Eirini Christodoulaki, Alvaro Ingles-Prieto, Evandro Ferrada, Fabian Frommelt, Shao Thing Teoh, Philipp Leippe, Gabriel Onea, Martin Pfeifer, Mariah Kohlbrenner, Lena Chang, Paul Selzer, Jürgen Reinhardt, Daniela Digles, Gerhard F Ecker, Tanja Osthushenrich, Aidan MacNamara, Anders Malarstig, David Hepworth, Giulio Superti-Furga
{"title":"Data- and knowledge-derived functional landscape of human solute carriers.","authors":"Ulrich Goldmann, Tabea Wiedmer, Andrea Garofoli, Vitaly Sedlyarov, Manuel Bichler, Ben Haladik, Gernot Wolf, Eirini Christodoulaki, Alvaro Ingles-Prieto, Evandro Ferrada, Fabian Frommelt, Shao Thing Teoh, Philipp Leippe, Gabriel Onea, Martin Pfeifer, Mariah Kohlbrenner, Lena Chang, Paul Selzer, Jürgen Reinhardt, Daniela Digles, Gerhard F Ecker, Tanja Osthushenrich, Aidan MacNamara, Anders Malarstig, David Hepworth, Giulio Superti-Furga","doi":"10.1038/s44320-025-00108-2","DOIUrl":"10.1038/s44320-025-00108-2","url":null,"abstract":"<p><p>The human solute carrier (SLC) superfamily of ~460 membrane transporters remains the largest understudied protein family despite its therapeutic potential. To advance SLC research, we developed a comprehensive knowledgebase that integrates systematic multi-omics data sets with selected curated information from public sources. We annotated SLC substrates through literature curation, compiled SLC disease associations using data mining techniques, and determined the subcellular localization of SLCs by combining annotations from public databases with an immunofluorescence imaging approach. This SLC-centric knowledge is made accessible to the scientific community via a web portal featuring interactive dashboards and visualization tools. Utilizing this systematically collected and curated resource, we computationally derived an integrated functional landscape for the entire human SLC superfamily. We identified clusters with distinct properties and established functional distances between transporters. Based on all available data sets and their integration, we assigned biochemical/biological functions to each SLC, making this study one of the largest systematic annotations of human gene function and a potential blueprint for future research endeavors.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"599-631"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The genetic interaction map of the human solute carrier superfamily.","authors":"Gernot Wolf, Philipp Leippe, Svenja Onstein, Ulrich Goldmann, Fabian Frommelt, Shao Thing Teoh, Enrico Girardi, Tabea Wiedmer, Giulio Superti-Furga","doi":"10.1038/s44320-025-00105-5","DOIUrl":"10.1038/s44320-025-00105-5","url":null,"abstract":"<p><p>Solute carriers (SLCs), the largest superfamily of transporter proteins in humans with about 450 members, control the movement of molecules across membranes. A typical human cell expresses over 200 different SLCs, yet their collective influence on cell phenotypes is not well understood due to overlapping substrate specificities and expression patterns. To address this, we performed systematic pairwise gene double knockouts using CRISPR-Cas12a and -Cas9 in human colon carcinoma cells. A total of 1,088,605 guide combinations were used to interrogate 35,421 SLC-SLC and SLC-enzyme double knockout combinations across multiple growth conditions, uncovering 1236 genetic interactions with a growth phenotype. Further exploration of an interaction between the mitochondrial citrate/malate exchanger SLC25A1 and the zinc transporter SLC39A1 revealed an unexpected role for SLC39A1 in metabolic reprogramming and anti-apoptotic signaling. This full-scale genetic interaction map of human SLC transporters is the backbone for understanding the intricate functional network of SLCs in cellular systems and generates hypotheses for pharmacological target exploitation in cancer and other diseases. The results are available at https://re-solute.eu/resources/dashboards/genomics/ .</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"531-559"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Samer Kadibalban, Axel Künstner, Torsten Schröder, Julius Zauleck, Oliver Witt, Georgios Marinos, Christoph Kaleta
{"title":"Metabolic modelling reveals increased autonomy and antagonism in type 2 diabetic gut microbiota.","authors":"A Samer Kadibalban, Axel Künstner, Torsten Schröder, Julius Zauleck, Oliver Witt, Georgios Marinos, Christoph Kaleta","doi":"10.1038/s44320-025-00100-w","DOIUrl":"10.1038/s44320-025-00100-w","url":null,"abstract":"<p><p>Type 2 diabetes (T2D) presents a global health concern, with evidence highlighting the role of the human gut microbiome in metabolic diseases. This study employs metabolic modelling to elucidate changes in host-microbiome interactions in T2D. Glucose levels, diet, 16S sequences and metadata were collected for 1866 individuals. In addition, microbial community models, and ecological interactions were simulated for the gut microbiomes. Our findings revealed a significant decrease in metabolic fluxes provided by the host's diet to the microbiome in T2D patients, accompanied by increased within-community exchanges. Moreover, the diabetic microbiomes shift towards increased exploitative ecological interactions at the expense of collaborative interactions. The reduced microbiome-to-host butyrate flux, along with decreased fluxes of amino acids (including tryptophan), nucleotides, and B vitamins from the host's diet, further highlight the dysregulation in microbial-host interactions in diabetes. In addition, microbiomes of T2D patients exhibit enrichment in energy metabolism, indicative of increased metabolic activity and antagonism. This study sheds light on the increased microbiome autonomy and antagonism accompanying diabetes, and provides candidate metabolic targets for intervention studies and experimental validation.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"720-731"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carles Foguet, Xilin Jiang, Scott C Ritchie, Elodie Persyn, Yu Xu, Chief Ben-Eghan, Henry J Taylor, Emanuele Di Angelantonio, John Danesh, Adam S Butterworth, Samuel A Lambert, Michael Inouye
{"title":"Metabolic reaction fluxes as amplifiers and buffers of risk alleles for coronary artery disease.","authors":"Carles Foguet, Xilin Jiang, Scott C Ritchie, Elodie Persyn, Yu Xu, Chief Ben-Eghan, Henry J Taylor, Emanuele Di Angelantonio, John Danesh, Adam S Butterworth, Samuel A Lambert, Michael Inouye","doi":"10.1038/s44320-025-00097-2","DOIUrl":"10.1038/s44320-025-00097-2","url":null,"abstract":"<p><p>Genome-wide association studies have identified thousands of variants associated with disease risk but the mechanism by which such variants contribute to disease remains largely unknown. Indeed, a major challenge is that variants do not act in isolation but rather in the framework of highly complex biological networks, such as the human metabolic network, which can amplify or buffer the effect of specific risk alleles on disease susceptibility. Here we use genetically predicted reaction fluxes to perform a systematic search for metabolic fluxes acting as buffers or amplifiers of coronary artery disease (CAD) risk alleles. Our analysis identifies 30 risk locus-reaction flux pairs with significant interaction on CAD susceptibility involving 18 individual reaction fluxes and 8 independent risk loci. Notably, many of these reactions are linked to processes with putative roles in the disease such as the metabolism of inflammatory mediators. In summary, this work establishes proof of concept that biochemical reaction fluxes can have non-additive effects with risk alleles and provides novel insights into the interplay between metabolism and genetic variation on disease susceptibility.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"676-695"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fuyuan Li, Shangzi Wang, Lian Chen, Ning Jiang, Xingdong Chen, Jin Li
{"title":"Systemic genome-epigenome analysis captures a lineage-specific super-enhancer for MYB in gastrointestinal adenocarcinoma.","authors":"Fuyuan Li, Shangzi Wang, Lian Chen, Ning Jiang, Xingdong Chen, Jin Li","doi":"10.1038/s44320-025-00098-1","DOIUrl":"10.1038/s44320-025-00098-1","url":null,"abstract":"<p><p>Gastrointestinal adenocarcinoma is a major cancer type for the digestive system, ranking as the top cause of cancer-related deaths worldwide. While there has been extensive research on mutations in protein-coding regions, the knowledge of the landscape of its non-coding regulatory elements is still insufficient. Combining the analysis of active enhancer profiles and genomic structural variation, we discovered and validated a lineage-specific super-enhancer for MYB in gastrointestinal adenocarcinoma. This super-enhancer is composed of a predominant enhancer e4 and several additional enhancers, whose transcriptional activity is regulated by the direct binding of HNF4A and MYB itself. Suppression of the super-enhancer downregulated the expression of MYB, inhibited downstream Notch signaling and prevented the development of gastrointestinal adenocarcinoma both in vitro and in vivo. Our study uncovers a mechanism driven by non-coding variations that regulate MYB expression in a lineage-specific manner, offering new insights into the carcinogenic mechanism and potential therapeutic strategies for gastrointestinal adenocarcinoma.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"696-719"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fabian Frommelt, Rene Ladurner, Ulrich Goldmann, Gernot Wolf, Alvaro Ingles-Prieto, Eva Lineiro-Retes, Zuzana Gelová, Ann-Katrin Hopp, Eirini Christodoulaki, Shao Thing Teoh, Philipp Leippe, Brianda L Santini, Manuele Rebsamen, Sabrina Lindinger, Iciar Serrano, Svenja Onstein, Christoph Klimek, Barbara Barbosa, Anastasiia Pantielieieva, Vojtech Dvorak, Thomas J Hannich, Julian Schoenbett, Gilles Sansig, Tamara A M Mocking, Jasper F Ooms, Adriaan P IJzerman, Laura H Heitman, Peter Sykacek, Juergen Reinhardt, André C Müller, Tabea Wiedmer, Giulio Superti-Furga
{"title":"The solute carrier superfamily interactome.","authors":"Fabian Frommelt, Rene Ladurner, Ulrich Goldmann, Gernot Wolf, Alvaro Ingles-Prieto, Eva Lineiro-Retes, Zuzana Gelová, Ann-Katrin Hopp, Eirini Christodoulaki, Shao Thing Teoh, Philipp Leippe, Brianda L Santini, Manuele Rebsamen, Sabrina Lindinger, Iciar Serrano, Svenja Onstein, Christoph Klimek, Barbara Barbosa, Anastasiia Pantielieieva, Vojtech Dvorak, Thomas J Hannich, Julian Schoenbett, Gilles Sansig, Tamara A M Mocking, Jasper F Ooms, Adriaan P IJzerman, Laura H Heitman, Peter Sykacek, Juergen Reinhardt, André C Müller, Tabea Wiedmer, Giulio Superti-Furga","doi":"10.1038/s44320-025-00109-1","DOIUrl":"10.1038/s44320-025-00109-1","url":null,"abstract":"<p><p>Solute carrier (SLC) transporters form a protein superfamily that enables transmembrane transport of diverse substrates including nutrients, ions and drugs. There are about 450 different SLCs, residing in a variety of subcellular membranes. Loss-of-function of an unusually high proportion of SLC transporters is genetically associated with a plethora of human diseases, making SLCs a rapidly emerging but challenging drug target class. Knowledge of their protein environment may elucidate the molecular basis for their functional integration with metabolic and cellular pathways and help conceive pharmacological interventions based on modulating proteostatic regulation. We aimed at obtaining a global survey of the SLC-protein interaction landscape and mapped the protein-protein interactions of 396 SLCs by interaction proteomics. We employed a functional assessment based on RNA interference of interactors in combination with measurement of protein stability and localization. As an example, we detail the role of a SLC16A6 phospho-degron and the contributions of PDZ-domain proteins LIN7C and MPP1 to the trafficking of SLC43A2. Overall, our work offers a resource for SLC-protein interactions for the scientific community.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"632-675"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tabea Wiedmer, Shao Thing Teoh, Eirini Christodoulaki, Gernot Wolf, Chengzhe Tian, Vitaly Sedlyarov, Abigail Jarret, Philipp Leippe, Fabian Frommelt, Alvaro Ingles-Prieto, Sabrina Lindinger, Barbara M G Barbosa, Svenja Onstein, Christoph Klimek, Julio Garcia, Iciar Serrano, Daniela Reil, Diana Santacruz, Mary Piotrowski, Stephen Noell, Christoph Bueschl, Huanyu Li, Gamma Chi, Stefan Mereiter, Tiago Oliveira, Josef M Penninger, David B Sauer, Claire M Steppan, Coralie Viollet, Kristaps Klavins, J Thomas Hannich, Ulrich Goldmann, Giulio Superti-Furga
{"title":"Metabolic mapping of the human solute carrier superfamily.","authors":"Tabea Wiedmer, Shao Thing Teoh, Eirini Christodoulaki, Gernot Wolf, Chengzhe Tian, Vitaly Sedlyarov, Abigail Jarret, Philipp Leippe, Fabian Frommelt, Alvaro Ingles-Prieto, Sabrina Lindinger, Barbara M G Barbosa, Svenja Onstein, Christoph Klimek, Julio Garcia, Iciar Serrano, Daniela Reil, Diana Santacruz, Mary Piotrowski, Stephen Noell, Christoph Bueschl, Huanyu Li, Gamma Chi, Stefan Mereiter, Tiago Oliveira, Josef M Penninger, David B Sauer, Claire M Steppan, Coralie Viollet, Kristaps Klavins, J Thomas Hannich, Ulrich Goldmann, Giulio Superti-Furga","doi":"10.1038/s44320-025-00106-4","DOIUrl":"10.1038/s44320-025-00106-4","url":null,"abstract":"<p><p>Solute carrier (SLC) transporters govern most of the chemical exchange across cellular membranes and are integral to metabolic regulation, which in turn is linked to cellular function and identity. Despite their key role, individual functions of the SLC superfamily members were not evaluated systematically. We determined the metabolic and transcriptional profiles upon SLC overexpression in knock-out or wild-type isogenic cell backgrounds for 378 SLCs and 441 SLCs, respectively. Targeted metabolomics provided a fingerprint of 189 intracellular metabolites, while transcriptomics offered insights into cellular programs modulated by SLC expression. Beyond the metabolic profiles of 102 SLCs directly related to their known substrates, we identified putative substrates or metabolic pathway connections for 71 SLCs without previously annotated bona fide substrates, including SLC45A4 as a new polyamine transporter. By comparing the molecular profiles, we identified functionally related SLC groups, including some with distinct impacts on osmolyte balancing and glycosylation. The assessment of functionally related human genes presented here may serve as a blueprint for other systematic studies and supports future investigations into the functional roles of SLCs.</p>","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"560-598"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Who controls the tariffs of a human cell?","authors":"Maximilian Billmann","doi":"10.1038/s44320-025-00112-6","DOIUrl":"10.1038/s44320-025-00112-6","url":null,"abstract":"","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"523-525"},"PeriodicalIF":8.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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