Research ExplorerPublicationsDecoding myofibroblast origins in human kidney fibrosis

Decoding myofibroblast origins in human kidney fibrosis

Standard

Decoding myofibroblast origins in human kidney fibrosis. / 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-Kanamari, 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.

In: NATURE, Vol. 589, No. 7841, 01.2021, p. 281-286.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Kuppe, C, Ibrahim, MM, Kranz, J, Zhang, X, Ziegler, S, Perales-Patón, J, Jansen, J, Reimer, KC, Smith, JR, Dobie, R, Wilson-Kanamari, JR, Halder, M, Xu, Y, Kabgani, N, Kaesler, N, Klaus, M, Gernhold, L, Puelles, VG, Huber, TB, Boor, P, Menzel, S, Hoogenboezem, RM, Bindels, EMJ, Steffens, J, Floege, J, Schneider, RK, Saez-Rodriguez, J, Henderson, NC & Kramann, R 2021, 'Decoding myofibroblast origins in human kidney fibrosis', NATURE, vol. 589, no. 7841, pp. 281-286. https://doi.org/10.1038/s41586-020-2941-1

APA

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-Kanamari, J. R., Halder, M., Xu, Y., Kabgani, N., Kaesler, N., Klaus, M., Gernhold, L., Puelles, V. G., Huber, T. B., ... Kramann, R. (2021). Decoding myofibroblast origins in human kidney fibrosis. NATURE, 589(7841), 281-286. https://doi.org/10.1038/s41586-020-2941-1

Vancouver

Kuppe C, Ibrahim MM, Kranz J, Zhang X, Ziegler S, Perales-Patón J et al. Decoding myofibroblast origins in human kidney fibrosis. NATURE. 2021 Jan;589(7841):281-286. https://doi.org/10.1038/s41586-020-2941-1

Bibtex

@article{79e9152e82cf4bbb8900fcc38aeb790d,
title = "Decoding myofibroblast origins in human kidney fibrosis",
abstract = "Kidney fibrosis is the hallmark of chronic kidney disease progression; however, at present no antifibrotic therapies exist1-3. The origin, functional heterogeneity and regulation of scar-forming cells that occur during human kidney fibrosis remain poorly understood1,2,4. 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.",
author = "Christoph Kuppe and Ibrahim, {Mahmoud M} and Jennifer Kranz and Xiaoting Zhang and Susanne Ziegler and Javier Perales-Pat{\'o}n and Jitske Jansen and Reimer, {Katharina C} and Smith, {James R} and Ross Dobie and Wilson-Kanamari, {John R} and Maurice Halder and Yaoxian Xu and Nazanin Kabgani and Nadine Kaesler and Martin Klaus and Lukas Gernhold and Puelles, {Victor G} and Huber, {Tobias B} and Peter Boor and Sylvia Menzel and Hoogenboezem, {Remco M} and Bindels, {Eric M J} and Joachim Steffens and J{\"u}rgen Floege and Schneider, {Rebekka K} and Julio Saez-Rodriguez and Henderson, {Neil C} and Rafael Kramann",
year = "2021",
month = jan,
doi = "10.1038/s41586-020-2941-1",
language = "English",
volume = "589",
pages = "281--286",
journal = "NATURE",
issn = "0028-0836",
publisher = "NATURE PUBLISHING GROUP",
number = "7841",

}

RIS

TY - JOUR

T1 - Decoding myofibroblast origins in human kidney fibrosis

AU - Kuppe, Christoph

AU - Ibrahim, Mahmoud M

AU - Kranz, Jennifer

AU - Zhang, Xiaoting

AU - Ziegler, Susanne

AU - Perales-Patón, Javier

AU - Jansen, Jitske

AU - Reimer, Katharina C

AU - Smith, James R

AU - Dobie, Ross

AU - Wilson-Kanamari, John R

AU - Halder, Maurice

AU - Xu, Yaoxian

AU - Kabgani, Nazanin

AU - Kaesler, Nadine

AU - Klaus, Martin

AU - Gernhold, Lukas

AU - Puelles, Victor G

AU - Huber, Tobias B

AU - Boor, Peter

AU - Menzel, Sylvia

AU - Hoogenboezem, Remco M

AU - Bindels, Eric M J

AU - Steffens, Joachim

AU - Floege, Jürgen

AU - Schneider, Rebekka K

AU - Saez-Rodriguez, Julio

AU - Henderson, Neil C

AU - Kramann, Rafael

PY - 2021/1

Y1 - 2021/1

N2 - Kidney fibrosis is the hallmark of chronic kidney disease progression; however, at present no antifibrotic therapies exist1-3. The origin, functional heterogeneity and regulation of scar-forming cells that occur during human kidney fibrosis remain poorly understood1,2,4. 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.

AB - Kidney fibrosis is the hallmark of chronic kidney disease progression; however, at present no antifibrotic therapies exist1-3. The origin, functional heterogeneity and regulation of scar-forming cells that occur during human kidney fibrosis remain poorly understood1,2,4. 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.

U2 - 10.1038/s41586-020-2941-1

DO - 10.1038/s41586-020-2941-1

M3 - SCORING: Journal article

C2 - 33176333

VL - 589

SP - 281

EP - 286

JO - NATURE

JF - NATURE

SN - 0028-0836

IS - 7841

ER -