[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-detail-169092-en":3,"doc-seo-169092-105":30,"detail-sidebar-cat-1-en-105":91},{"code":4,"msg":5,"data":6},0,"success",{"doc_id":7,"user_id":8,"nickname":9,"user_avatar":10,"doc_module":11,"category_id":12,"category_name":13,"doc_title":14,"doc_description":15,"doc_content":16,"file_id":17,"file_url":18,"file_type":19,"file_size":20,"view_count":4,"is_deleted":4,"is_public":11,"is_downloadable":11,"audit_status":11,"page_count":21,"language":22,"language_code":23,"site_id":24,"html_lang":23,"table_of_contents":25,"faqs":26,"seo_title":27,"seo_description":15,"update_tm":28,"read_time":29},169092,4810365810221,"Aurora","https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d",1,21,"Paper Templates","Decoding myofibroblast origins in human kidney fibrosis","Kidney fibrosis drives chronic kidney disease progression, yet no effective antifibrotic therapies exist because the origin, functional heterogeneity, and regulation of scar-forming cells in humans remain incompletely defined. Single-cell RNA-seq profiled proximal and non-proximal tubule cells from healthy and fibrotic human kidneys to build an unbiased cellular map. Matrix-producing pericyte and fibroblast subpopulations were identified as main sources of myofibroblasts. Mouse genetic fate-tracing, time-course scRNA-seq and ATAC-seq, plus human spatial transcriptomics, functionally validated myofibroblast differentiation and heterogeneity, enabling target discovery.","Decoding myofibroblast origins in human kidney fibrosis\nAuthors:\nChristoph Kuppe,1,2# Mahmoud M Ibrahim,1,2,3,# Jennifer Kranz,4,5 Xiaoting Zhang,1,2 Susanne Ziegler,1,2  Javier Perales-Patón,2,6,7 Jitske Jansen,2,8,9 Katharina C. Reimer,1,2,10 James R. Smith,11 Ross Dobie,11  John R. Wilson-Kanamari,11 Maurice Halder,1,2  Yaoxian Xu,2 Nazanin Kabgani,2 Nadine Kaesler,1,2 Martin Klaus,12 Lukas Gernhold,12 Victor G. Puelles12,13 Tobias B. Huber,21 Peter Boor,1,14 Sylvia Menzel,2   Remco M.  Hoogenboezem,15 Eric M.J. Bindels,15 Joachim Steffens,4 Jürgen Floege,1 Rebekka K Schneider,10,15 Julio Saez-Rodriguez,6,7,16 Neil C Henderson11,17* and Rafael Kramann1,2,18*\nAffiliations:\n1Division of Nephrology and Clinical Immunology, RWTH Aachen University, Aachen, Germany\n2Institute of Experimental Medicine and Systems Biology, RWTH Aachen University, Germany\n3Present address: Bayer Pharma AG, Germany\n4 Department of Urology and Paediatric Urology, St. Antonius Hospital, Eschweiler, Germany\n5Department of Urology and Kidney Transplantation, Martin-Luther-University, Halle (Saale), Germany\n6Heidelberg University, Faculty of Medicine, and Heidelberg University Hospital, Institute for Computational Biomedicine, Bioquant, Heidelberg, Germany\n7Joint Research Center for Computational Biomedicine, RWTH Aachen University Hospital, 52074 Aachen, Germany\n8Department of Pathology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.\n9Department of Pediatric Nephrology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Amalia Children's Hospital, Nijmegen, The Netherlands.\n10Institute for Biomedical Technologies, Department of Cell Biology, RWTH Aachen University, Aachen, Germany\n11Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.\n12III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany\n13Department of Anatomy and Developmental Biology, Monash University, Melbourne, Australia.Gman\n14Department of Pathology, RWTH Aachen University, Aachen, Germany\n15Department of Hematology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.\n16Molecular Medicine Partnership Unit, European Molecular Biology Laboratory and Heidelberg University, Heidelberg, Germany\n17MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh, UK.\n18Department of Internal Medicine, Nephrology and Transplantation, Erasmus Medical Center, Rotterdam, The Netherlands\n# These authors contributed equally to this work. * Co-senior authors\nCorrespondence to:\nRafael Kramann, MD, PhD\nDepartment of Experimental Medicine and Systems Biology\nand Division of Nephrology and Clinical Immunology,\nMedical Faculty RWTH Aachen University,\nPauwelsstrasse 30, 52074 Aachen, Germany\nPhone.: 0049-241-80 37750\nFax.: +49-241-80-82446 E-mail: \u0013 HYPERLINK \"mailto:rkramann@gmx.net\" \\h \u0014rkramann@gmx.net\u0015\nAbstract\nKidney fibrosis is the hallmark of chronic kidney disease progression, however, currently no antifibrotic therapies exist. This is largely because the origin, functional heterogeneity and regulation of scar-forming cells during human kidney fibrosis remains poorly understood. Here, using single cell RNA-seq, we profiled the transcriptomes of proximal tubule and non-proximal tubule cells in healthy and fibrotic human kidneys to map the entire human kidney in an unbiased approach. This enabled mapping of all matrix-producing cells at high resolution, revealing distinct subpopulations of pericytes and fibroblasts as the major cellular sources of scar forming myofibroblasts during human kidney fibrosis. We used genetic fate-tracing, time-course single cell RNA-seq and ATAC-seq experiments in mice, and spatial transcriptomics in human kidney fibrosis to functionally interrogate these findings, shedding new light on the origin, heterogeneity and differentiati","cbCaiczT2dUBVAs4","https://ap.wps.com/l/cbCaiczT2dUBVAs4","docx",85423,30,"English","en",105,"# Abstract\n# Single cell atlas of human chronic kidney disease\n# Decoding myofibroblast origins in human kidney fibrosis","[{\"question\":\"Why are there currently no approved antifibrotic therapies for kidney fibrosis?\",\"answer\":\"Because the origin, functional heterogeneity, and regulation of scar-forming cells during human kidney fibrosis are still poorly understood.\"},{\"question\":\"How did the study characterize cells involved in human kidney fibrosis?\",\"answer\":\"It used single-cell RNA-seq to profile transcriptomes of proximal and non-proximal tubule cells in healthy and fibrotic human kidneys, enabling high-resolution mapping of matrix-producing cells.\"},{\"question\":\"What cellular sources were identified for scar-forming myofibroblasts?\",\"answer\":\"Distinct subpopulations of pericytes and fibroblasts were revealed as major sources of scar-forming myofibroblasts during human kidney fibrosis.\"}]","Decoding myofibroblast origins in human kidney fibrosis | 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are there currently no approved antifibrotic therapies for kidney fibrosis?","Question",{"text":75,"@type":76},"Because the origin, functional heterogeneity, and regulation of scar-forming cells during human kidney fibrosis are still poorly understood.","Answer",{"name":78,"@type":73,"acceptedAnswer":79},"How did the study characterize cells involved in human kidney fibrosis?",{"text":80,"@type":76},"It used single-cell RNA-seq to profile transcriptomes of proximal and non-proximal tubule cells in healthy and fibrotic human kidneys, enabling high-resolution mapping of matrix-producing cells.",{"name":82,"@type":73,"acceptedAnswer":83},"What cellular sources were identified for scar-forming myofibroblasts?",{"text":84,"@type":76},"Distinct subpopulations of pericytes and fibroblasts were revealed as major sources of scar-forming myofibroblasts during human kidney 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