Evidence map›Paper›PMID 38340720›Full record

ArticleDevelopmental cell2024

Identification of a core transcriptional program driving the human renal mesenchymal-to-epithelial transition.

John-Poul Ng-Blichfeldt, Benjamin J Stewart, Menna R Clatworthy, Julie M Williams, Katja Röper

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Epigenetic regulation of kidney development.Nature reviews. Nephrology · 2026
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  11. International journal of molecular sciences · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

John-Poul Ng-BlichfeldtMRC-Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK.
Benjamin J StewartMolecular Immunity Unit, Department of Medicine, MRC-Laboratory of Molecular Biology, University of Cambridge, Cambridge, UK; Cellular Genetics, Wellcome Sanger Institute, Hinxton, UK.
Menna R ClatworthyMolecular Immunity Unit, Department of Medicine, MRC-Laboratory of Molecular Biology, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology and Infectious Diseases, University of Cambridge, Cambridge, UK.
Julie M WilliamsBioscience Renal, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Katja RöperMRC-Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. Electronic address: kroeper@mrc-lmb.cam.ac.uk.
MRC Laboratory of Molecular Biology · GBAstraZeneca (Sweden) · SE

Funding

Medical Research Council MC_U105178780Medical Research Council MC_UP_1201/11Medical Research Council U105178780NIH HHS NIHR203312Wellcome TrustWellcome Trust 216366/Z/19/ZWellcome Trust 220268/Z/20/Z
6 · The paper itself

Abstract

During kidney development, nephron epithelia arise de novo from fate-committed mesenchymal progenitors through a mesenchymal-to-epithelial transition (MET). Downstream of fate specification, transcriptional mechanisms that drive establishment of epithelial morphology are poorly understood. We used human iPSC-derived renal organoids, which recapitulate nephrogenesis, to investigate mechanisms controlling renal MET. Multi-ome profiling via snRNA-seq and ATAC-seq of organoids identified dynamic changes in gene expression and chromatin accessibility driven by activators and repressors throughout MET. CRISPR interference identified that paired box 8 (PAX8) is essential for initiation of MET in human renal organoids, contrary to in vivo mouse studies, likely by activating a cell-adhesion program. While Wnt/β-catenin signaling specifies nephron fate, we find that it must be attenuated to allow hepatocyte nuclear factor 1-beta (HNF1B) and TEA-domain (TEAD) transcription factors to drive completion of MET. These results identify the interplay between fate commitment and morphogenesis in the developing human kidney, with implications for understanding both developmental kidney diseases and aberrant epithelial plasticity following adult renal tubular injury.

Indexed as

KidneyNephronsAnimalsCell DifferentiationEpithelial-Mesenchymal TransitionHumansMiceSignal TransductionTranscription FactorsTranscription Factorsepithelial polaritykidney developmentmesenchymal-to-epithelial transitionorganoidstranscriptional regulation

Identifiers

PMID38340720
PMCPMC7616043
OpenAlexW4391684258

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.