Pub Date : 2026-01-06DOI: 10.1038/s44161-025-00761-8
Michael R. Murphy, Mythily Ganapathi, Esther R. Rotlevi, Teresa M. Lee, Joshua M. Fisher, Megha V. Patel, Parul Jayakar, Amanda Buchanan, Alyssa L. Rippert, Rebecca C. Ahrens-Nicklas, Divya Nair, Shalini S. Nayak, Aakanksha Anand, Anju Shukla, Rajesh K. Soni, Yue Yin, Feiyue Yang, Enrique J. Garcia, Muredach P. Reilly, Wendy K. Chung, Xuebing Wu
The heart uses a muscle-specific ribosome in cardiomyocytes, where the ribosomal protein RPL3 is replaced by its paralog RPL3L. Rare biallelic RPL3L mutations cause fatal neonatal dilated cardiomyopathy, yet the mechanisms that link genotype to heart failure are unclear. Despite the recessive inheritance pattern in humans, Rpl3l knockout mice show no overt cardiac phenotype, probably because of compensatory RPL3 upregulation through unknown mechanisms. Here we report four additional cases and propose a unifying pathogenetic model by integrating human genetics, patient tissues and isogenic cell models. Affected individuals typically carry one of two recurrent hotspot missense variants paired with a private allele. Whereas non-hotspot variants phenocopy knockout and allow RPL3 compensation, hotspot variants induce nucleolar protein aggregation, disrupt rRNA processing and block compensation by preserving the role of RPL3L in repressing RPL3 via unproductive splicing. These findings establish combined loss-of-function and gain-of-function mechanisms for RPL3L-associated cardiomyopathy and inform genetic screening, diagnosis and therapeutic development. Murphy et al. reveal a unifying pathogenetic mechanism according to which diverse mutations in the muscle-specific ribosomal protein RPL3L cause severe neonatal dilated cardiomyopathy, establishing a framework for interpreting the growing spectrum of RPL3L variants.
{"title":"Pathogenetic mechanisms of muscle-specific ribosomes in dilated cardiomyopathy","authors":"Michael R. Murphy, Mythily Ganapathi, Esther R. Rotlevi, Teresa M. Lee, Joshua M. Fisher, Megha V. Patel, Parul Jayakar, Amanda Buchanan, Alyssa L. Rippert, Rebecca C. Ahrens-Nicklas, Divya Nair, Shalini S. Nayak, Aakanksha Anand, Anju Shukla, Rajesh K. Soni, Yue Yin, Feiyue Yang, Enrique J. Garcia, Muredach P. Reilly, Wendy K. Chung, Xuebing Wu","doi":"10.1038/s44161-025-00761-8","DOIUrl":"10.1038/s44161-025-00761-8","url":null,"abstract":"The heart uses a muscle-specific ribosome in cardiomyocytes, where the ribosomal protein RPL3 is replaced by its paralog RPL3L. Rare biallelic RPL3L mutations cause fatal neonatal dilated cardiomyopathy, yet the mechanisms that link genotype to heart failure are unclear. Despite the recessive inheritance pattern in humans, Rpl3l knockout mice show no overt cardiac phenotype, probably because of compensatory RPL3 upregulation through unknown mechanisms. Here we report four additional cases and propose a unifying pathogenetic model by integrating human genetics, patient tissues and isogenic cell models. Affected individuals typically carry one of two recurrent hotspot missense variants paired with a private allele. Whereas non-hotspot variants phenocopy knockout and allow RPL3 compensation, hotspot variants induce nucleolar protein aggregation, disrupt rRNA processing and block compensation by preserving the role of RPL3L in repressing RPL3 via unproductive splicing. These findings establish combined loss-of-function and gain-of-function mechanisms for RPL3L-associated cardiomyopathy and inform genetic screening, diagnosis and therapeutic development. Murphy et al. reveal a unifying pathogenetic mechanism according to which diverse mutations in the muscle-specific ribosomal protein RPL3L cause severe neonatal dilated cardiomyopathy, establishing a framework for interpreting the growing spectrum of RPL3L variants.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"51-66"},"PeriodicalIF":10.8,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00761-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913980","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}
Pub Date : 2026-01-05DOI: 10.1038/s44161-025-00762-7
Junichi Saito, Jui M. Dave, Eunate Gallardo-Vara, Nandhini Sadagopan, Inamul Kabir, George Tellides, Robert K. Riemer, Zsolt Urban, Sarah Spiegel, Timothy Hla, Daniel M. Greif
Deficiency of elastin (ELN), the major component of elastic fibers, leads to excess smooth muscle cells (SMCs), which characterizes arterial diseases (for example, supravalvular aortic stenosis (SVAS)) as well as physiological ductus arteriosus (DA) closure. Here we demonstrate that sphingosine kinase 1 (SPHK1) is a key node in these contexts. Sphk1 is the most upregulated transcript in Eln(−/−) aortic SMCs at embryonic day 15.5 when these cells are initially hyperproliferative. The aorta of humans with SVAS also upregulates SPHK1. Reduced ELN increases levels of transcription factor early growth response 1, resulting in increased SPHK1 levels. SMC-specific Sphk1 deletion or pharmacological inhibition of SPHK1 attenuates SMC proliferation and mitigates aortic disease. Furthermore, treatment with a SPHK1 inhibitor reduces DA SMC accumulation, leading to DA patency in wild-type mice. These findings indicate that inhibiting SPHK1 may be a therapeutic strategy for SVAS and select congenital heart diseases in which patent DA maintains circulation. Saito et al. identify sphingosine kinase 1 as a critical regulator of physiological ductus arteriosus closure and pathological supravalvular aortic stenosis through its role in smooth muscle cell proliferation and propose potential therapeutics.
{"title":"Sphingosine kinase 1 is integral for elastin deficiency-induced arterial hypermuscularization","authors":"Junichi Saito, Jui M. Dave, Eunate Gallardo-Vara, Nandhini Sadagopan, Inamul Kabir, George Tellides, Robert K. Riemer, Zsolt Urban, Sarah Spiegel, Timothy Hla, Daniel M. Greif","doi":"10.1038/s44161-025-00762-7","DOIUrl":"10.1038/s44161-025-00762-7","url":null,"abstract":"Deficiency of elastin (ELN), the major component of elastic fibers, leads to excess smooth muscle cells (SMCs), which characterizes arterial diseases (for example, supravalvular aortic stenosis (SVAS)) as well as physiological ductus arteriosus (DA) closure. Here we demonstrate that sphingosine kinase 1 (SPHK1) is a key node in these contexts. Sphk1 is the most upregulated transcript in Eln(−/−) aortic SMCs at embryonic day 15.5 when these cells are initially hyperproliferative. The aorta of humans with SVAS also upregulates SPHK1. Reduced ELN increases levels of transcription factor early growth response 1, resulting in increased SPHK1 levels. SMC-specific Sphk1 deletion or pharmacological inhibition of SPHK1 attenuates SMC proliferation and mitigates aortic disease. Furthermore, treatment with a SPHK1 inhibitor reduces DA SMC accumulation, leading to DA patency in wild-type mice. These findings indicate that inhibiting SPHK1 may be a therapeutic strategy for SVAS and select congenital heart diseases in which patent DA maintains circulation. Saito et al. identify sphingosine kinase 1 as a critical regulator of physiological ductus arteriosus closure and pathological supravalvular aortic stenosis through its role in smooth muscle cell proliferation and propose potential therapeutics.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"34-50"},"PeriodicalIF":10.8,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-05DOI: 10.1038/s44161-025-00763-6
Odai Darawshi, Besim Ogretmen
Defects in elastin trigger hyperproliferation of smooth muscle cells, which leads to arterial and congenital heart diseases. Research now shows that elastin deficiency induces SPHK1 and S1P signaling by EGR1 in SMCs, and inhibitors of SPHK1 or S1PR1 attenuate smooth muscle cell proliferation and mitigate aortic disease.
{"title":"Sphingolipid signaling links elastin deficiency to arterial hyper-muscularization and congenital heart disease","authors":"Odai Darawshi, Besim Ogretmen","doi":"10.1038/s44161-025-00763-6","DOIUrl":"10.1038/s44161-025-00763-6","url":null,"abstract":"Defects in elastin trigger hyperproliferation of smooth muscle cells, which leads to arterial and congenital heart diseases. Research now shows that elastin deficiency induces SPHK1 and S1P signaling by EGR1 in SMCs, and inhibitors of SPHK1 or S1PR1 attenuate smooth muscle cell proliferation and mitigate aortic disease.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"10-11"},"PeriodicalIF":10.8,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s44161-025-00760-9
Jennifer L. Hall
Most drugs in phase 2 trials fail to reach regulatory approval. By leveraging machine learning to identify connections between different types of data, including genes, diseases, medications, existing drugs and images, a new approach is shown to increase the level of evidence in identifying drug targets for cardiovascular disease.
{"title":"Connecting to improve drug discovery","authors":"Jennifer L. Hall","doi":"10.1038/s44161-025-00760-9","DOIUrl":"10.1038/s44161-025-00760-9","url":null,"abstract":"Most drugs in phase 2 trials fail to reach regulatory approval. By leveraging machine learning to identify connections between different types of data, including genes, diseases, medications, existing drugs and images, a new approach is shown to increase the level of evidence in identifying drug targets for cardiovascular disease.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"8-9"},"PeriodicalIF":10.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s44161-025-00766-3
The transcription factor TBX5 regulates early cardiac progenitor cells and genes that encode essential patterning cues for the correct formation of the interventricular septum and separation of cardiac chambers in mice. Disruption of a compartment boundary at the developing interventricular septum reveals potential mechanisms that might underlie some congenital heart defects.
{"title":"Insights on the origins of the interventricular septum","authors":"","doi":"10.1038/s44161-025-00766-3","DOIUrl":"10.1038/s44161-025-00766-3","url":null,"abstract":"The transcription factor TBX5 regulates early cardiac progenitor cells and genes that encode essential patterning cues for the correct formation of the interventricular septum and separation of cardiac chambers in mice. Disruption of a compartment boundary at the developing interventricular septum reveals potential mechanisms that might underlie some congenital heart defects.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"14-15"},"PeriodicalIF":10.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s44161-025-00767-2
Correlating the mitochondrial membrane potential with the redox status of endogenous mitochondrial cytochromes in vitro enabled the real-time determination of the mitochondrial membrane potential in an isolated perfused mouse heart. This model was used to provide insights into cardiac ischemia–reperfusion injury.
{"title":"Real-time measurement of the mitochondrial membrane potential in the intact mouse heart","authors":"","doi":"10.1038/s44161-025-00767-2","DOIUrl":"10.1038/s44161-025-00767-2","url":null,"abstract":"Correlating the mitochondrial membrane potential with the redox status of endogenous mitochondrial cytochromes in vitro enabled the real-time determination of the mitochondrial membrane potential in an isolated perfused mouse heart. This model was used to provide insights into cardiac ischemia–reperfusion injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"12-13"},"PeriodicalIF":10.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s44161-025-00764-5
Elisa Martini
{"title":"Loss of function of the obesity-associated gene MC4R reduces cardiovascular risk and increases lipid clearance","authors":"Elisa Martini","doi":"10.1038/s44161-025-00764-5","DOIUrl":"10.1038/s44161-025-00764-5","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"4-4"},"PeriodicalIF":10.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1038/s44161-025-00755-6
Irfan S. Kathiriya, Martin H. Dominguez, Kavitha S. Rao, Jonathon M. Muncie-Vasic, W. Patrick Devine, Kevin M. Hu, Swetansu K. Hota, Bayardo I. Garay, Diego Quintero, Piyush Goyal, Megan N. Matthews, Reuben Thomas, Tatyana Sukonnik, Dario Miguel-Perez, Sarah Winchester, Emily F. Brower, André Forjaz, Pei-Hsun Wu, Denis Wirtz, Ashley L. Kiemen, Benoit G. Bruneau
Failure of septation of the interventricular septum (IVS) is the most common congenital heart defect, but mechanisms for patterning the IVS are largely unknown. Here we show that a Tbx5+/Mef2cAHF+ progenitor lineage forms a compartment boundary bisecting the IVS. This coordinated population originates at a first and second heart field interface. Ablation of Tbx5+/Mef2cAHF+ progenitors causes IVS disorganization, right ventricular hypoplasia and mixing of IVS lineages. Reduced dosage of the congenital heart defect transcription factor TBX5 disrupts boundary position and integrity, resulting in ventricular septation defects and patterning defects, including misexpression of Slit2 and Ntn1, which encode guidance cues. Reducing NTN1 dosage partly rescues cardiac defects in Tbx5 mutant embryos. Loss of Slit2 or Ntn1 causes ventricular septation defects and perturbed septal lineage distributions. Thus, we identify Tbx5 as a candidate selector gene, directing progenitors and regulating essential cues, to pattern a compartment boundary for proper cardiac septation, revealing mechanisms for cardiac birth defects. Kathiriya et al. identify a cardiac progenitor lineage with expression of Tbx5 and anterior heart field-specific expression of Mef2c that bisects the intraventricular septum during development and show that alterations in this lineage lead to congenital heart defects in mice.
{"title":"A disrupted compartment boundary underlies abnormal cardiac patterning and congenital heart defects","authors":"Irfan S. Kathiriya, Martin H. Dominguez, Kavitha S. Rao, Jonathon M. Muncie-Vasic, W. Patrick Devine, Kevin M. Hu, Swetansu K. Hota, Bayardo I. Garay, Diego Quintero, Piyush Goyal, Megan N. Matthews, Reuben Thomas, Tatyana Sukonnik, Dario Miguel-Perez, Sarah Winchester, Emily F. Brower, André Forjaz, Pei-Hsun Wu, Denis Wirtz, Ashley L. Kiemen, Benoit G. Bruneau","doi":"10.1038/s44161-025-00755-6","DOIUrl":"10.1038/s44161-025-00755-6","url":null,"abstract":"Failure of septation of the interventricular septum (IVS) is the most common congenital heart defect, but mechanisms for patterning the IVS are largely unknown. Here we show that a Tbx5+/Mef2cAHF+ progenitor lineage forms a compartment boundary bisecting the IVS. This coordinated population originates at a first and second heart field interface. Ablation of Tbx5+/Mef2cAHF+ progenitors causes IVS disorganization, right ventricular hypoplasia and mixing of IVS lineages. Reduced dosage of the congenital heart defect transcription factor TBX5 disrupts boundary position and integrity, resulting in ventricular septation defects and patterning defects, including misexpression of Slit2 and Ntn1, which encode guidance cues. Reducing NTN1 dosage partly rescues cardiac defects in Tbx5 mutant embryos. Loss of Slit2 or Ntn1 causes ventricular septation defects and perturbed septal lineage distributions. Thus, we identify Tbx5 as a candidate selector gene, directing progenitors and regulating essential cues, to pattern a compartment boundary for proper cardiac septation, revealing mechanisms for cardiac birth defects. Kathiriya et al. identify a cardiac progenitor lineage with expression of Tbx5 and anterior heart field-specific expression of Mef2c that bisects the intraventricular septum during development and show that alterations in this lineage lead to congenital heart defects in mice.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"67-83"},"PeriodicalIF":10.8,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00755-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145859468","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}
Pub Date : 2025-12-29DOI: 10.1038/s44161-025-00757-4
Khaled Rjoob, Kathryn A. McGurk, Sean L. Zheng, Lara Curran, Mahmoud Ibrahim, Lingyao Zeng, Vladislav Kim, Shamin Tahasildar, Soodeh Kalaie, Deva S. Senevirathne, Parisa Gifani, Vladimir Losev, Jin Zheng, Wenjia Bai, Antonio de Marvao, James S. Ware, Christian Bender, Declan P. O’Regan
Understanding gene–disease associations is important for uncovering pathological mechanisms and identifying potential therapeutic targets. Knowledge graphs can represent and integrate data from multiple biomedical sources, but lack individual-level information on target organ structure and function. Here we develop CardioKG, a knowledge graph that integrates over 200,000 computer vision-derived cardiovascular phenotypes from biomedical images with data extracted from 18 biological databases to model over a million relationships. We used a variational graph auto-encoder to generate node embeddings from the knowledge graph to predict gene–disease associations, assess druggability and identify drug repurposing strategies. The model predicted genetic associations and therapeutic opportunities for leading causes of cardiovascular disease, which were associated with improved survival. Candidate therapies included methotrexate for heart failure and gliptins for atrial fibrillation, and the addition of imaging data enhanced pathway discovery. These capabilities support the use of biomedical imaging to enhance graph-structured models for identifying treatable disease mechanisms. Rjoob et al. develop CardioKG, a knowledge graph built on cardiac imaging traits to identify genetic associations and potential therapeutic strategies and drug repurposing opportunities for cardiovascular diseases.
{"title":"A multimodal vision knowledge graph of cardiovascular disease","authors":"Khaled Rjoob, Kathryn A. McGurk, Sean L. Zheng, Lara Curran, Mahmoud Ibrahim, Lingyao Zeng, Vladislav Kim, Shamin Tahasildar, Soodeh Kalaie, Deva S. Senevirathne, Parisa Gifani, Vladimir Losev, Jin Zheng, Wenjia Bai, Antonio de Marvao, James S. Ware, Christian Bender, Declan P. O’Regan","doi":"10.1038/s44161-025-00757-4","DOIUrl":"10.1038/s44161-025-00757-4","url":null,"abstract":"Understanding gene–disease associations is important for uncovering pathological mechanisms and identifying potential therapeutic targets. Knowledge graphs can represent and integrate data from multiple biomedical sources, but lack individual-level information on target organ structure and function. Here we develop CardioKG, a knowledge graph that integrates over 200,000 computer vision-derived cardiovascular phenotypes from biomedical images with data extracted from 18 biological databases to model over a million relationships. We used a variational graph auto-encoder to generate node embeddings from the knowledge graph to predict gene–disease associations, assess druggability and identify drug repurposing strategies. The model predicted genetic associations and therapeutic opportunities for leading causes of cardiovascular disease, which were associated with improved survival. Candidate therapies included methotrexate for heart failure and gliptins for atrial fibrillation, and the addition of imaging data enhanced pathway discovery. These capabilities support the use of biomedical imaging to enhance graph-structured models for identifying treatable disease mechanisms. Rjoob et al. develop CardioKG, a knowledge graph built on cardiac imaging traits to identify genetic associations and potential therapeutic strategies and drug repurposing opportunities for cardiovascular diseases.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"18-33"},"PeriodicalIF":10.8,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00757-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145859527","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}
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