Cited by 770Chronic Kidney Disease and DiabetesAcute Kidney Injury ResearchRenal Diseases and Glomerulopathies

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Decoding myofibroblast origins in human kidney fibrosis

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Kuppe, Christoph, Ibrahim, Mahmoud M., Kranz, Jennifer, Zhang, Xiaoting, Ziegler, Susanne, Perales-Patón, Javier, Jansen, Jitske, Reimer, Katharina C., Smith, James R., Dobie, Ross, Wilson-Kanamori, John R., Halder, Maurice, Xu, Yaoxian, Kabgani, Nazanin, Kaesler, Nadine, Klaus, Martin, Gernhold, Lukas, Puelles, Victor G., Huber, Tobias B., Boor, Peter, Menzel, Sylvia, Hoogenboezem, Remco M., Bindels, Eric M. J., Steffens, Joachim, Floege, Jürgen, Schneider, Rebekka K., Saez-Rodriguez, Julio, Henderson, Neil C., Kramann, Rafael·2021·Nature

DOI 10.1038/s41586-020-2941-1PMC PMC7611626

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Abstract

Kidney fibrosis is the hallmark of chronic kidney disease progression; however, at present no antifibrotic therapies exist 1-3. The origin, functional heterogeneity and regulation of scar-forming cells that occur during human kidney fibrosis remain poorly understood 1,2,4. Here, using single-cell RNA sequencing, we profiled the transcriptomes of cells from the proximal and non-proximal tubules of healthy and fibrotic human kidneys to map the entire human kidney. This analysis enabled us to map all matrix-producing cells at high resolution, and to identify distinct subpopulations of pericytes and fibroblasts as the main cellular sources of scar-forming myofibroblasts during human kidney fibrosis. We used genetic fate-tracing, time-course single-cell RNA sequencing and ATAC-seq (assay for transposase-accessible chromatin using sequencing) experiments in mice, and spatial transcriptomics in human kidney fibrosis, to shed light on the cellular origins and differentiation of human kidney myofibroblasts and their precursors at high resolution. Finally, we used this strategy to detect potential therapeutic targets, and identified NKD2 as a myofibroblast-specific target in human kidney fibrosis.

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Authors: Kuppe, C., Ibrahim, M. M., Kranz, J., Zhang, X., Ziegler, S., Perales-Patón, J., Jansen, J., Reimer, K. C., Smith, J. R., Dobie, R., Wilson-Kanamori, J. R., Halder, M., Xu, Y., Kabgani, N., Kaesler, N., Klaus, M., Gernhold, L., Puelles, V. G., Huber, T. B., Boor, P., Menzel, S., Hoogenboezem, R. M., Bindels, E. M. J., Steffens, J., Floege, J., Schneider, R. K., Saez-Rodriguez, J., Henderson, N. C., & Kramann, R.
Affiliations: RWTH Aachen University (DE)
Sankt-Antonius-Hospital Eschweiler (DE)
Heidelberg University (DE)
Radboud University Nijmegen (NL)
Centre for Inflammation Research (GB)
University Medical Center Hamburg-Eppendorf (DE)
Erasmus MC Cancer Institute (NL)
Erasmus MC (NL)
Corresponding author: Kramann, Rafael
ORCID: Kuppe, Christoph
Ibrahim, Mahmoud M.
Kranz, Jennifer
Zhang, Xiaoting
Ziegler, Susanne
Perales-Patón, Javier
Jansen, Jitske
Reimer, Katharina C.
Smith, James R.
Dobie, Ross
Wilson-Kanamori, John R.
Halder, Maurice
Kaesler, Nadine
Klaus, Martin
Puelles, Victor G.
Huber, Tobias B.
Boor, Peter
Hoogenboezem, Remco M.
Bindels, Eric M. J.
Floege, Jürgen
Schneider, Rebekka K.
Saez-Rodriguez, Julio
Henderson, Neil C.
Kramann, Rafael
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2020-11-11
Volume: 589
Issue: 7841
Pages: 281-286
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/s41586-020-2941-1
PMC: PMC7611626
OpenAlex: W3104014715
Cited by: 769
References: 86
Citations by year: 2026: 147 · 2025: 128 · 2024: 148 · 2023: 139 · 2022: 115 · 2021: 87 · 2020: 3
FWCI: 54.23
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: other-oa
www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature (publishedVersion)
EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, other-oa)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, other-oa)
RePEc: Research Papers in Economics (submittedVersion)
Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, cc-by)
Funders: European Hematology Association
Wellcome Trust (219542/Z/19/Z, 104366/Z/14/Z)
British Heart Foundation (RM/17/3/33381, RE/18/5/34216)
Deutsche Forschungsgemeinschaft (TRR57, SFBTRR219, BO3755/3‐1, TRR219, CRC 1192, SFB‐TRR57, SCHN 1188/5-1, BO3755/6-1, CRU344)
Bundesministerium für Bildung und Forschung (01GM1901A, STOP‐FSGS 01GM1901A)
Else Kröner-Fresenius-Stiftung
RWTH Aachen University (SFBTRR219, O3-11)
Medical Research Council
H2020 European Research Council (677448)
Topics: Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Keywords: renal fibrosis, myofibroblast origin, chronic kidney disease, pericytes, fibroblasts, proximal tubule, NKD2, cell fate tracing, single-cell transcriptomics, spatial transcriptomics, ATAC-seq
MeSH terms: RNA-Seq, Animals, Calcium-Binding Proteins, Cell Differentiation, Extracellular Matrix, Female, Fibroblasts, Fibrosis, Humans, Kidney Tubules, Male, Mesoderm, Case-Control Studies, Cell Lineage, Pericytes, Receptor, Platelet-Derived Growth Factor alpha, Receptor, Platelet-Derived Growth Factor beta, Adaptor Proteins, Signal Transducing, Mice, Renal Insufficiency, Chronic, Myofibroblasts, Single-Cell Analysis, Transcriptome

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