Evidence map›Paper›PMID 32978267›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Kidney Single-Cell Atlas Reveals Myeloid Heterogeneity in Progression and Regression of Kidney Disease.

Bryan R Conway, Eoin D O'Sullivan, Carolynn Cairns, James O'Sullivan, Daniel J Simpson, Angela Salzano, Katie Connor, Peng Ding, Duncan Humphries, Kevin Stewart and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 2 pooled it
8.8field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 2 syntheses or guidelines pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026
    Review
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  6. STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
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  15. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

83 more citing papers are in PubMed but not listed here.

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

19 authors at 4 institutions in 1 country.

Bryan R ConwayCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom Laura.Denby@ed.ac.uk Tamir.Chandra@ed.ac.uk.
Eoin D O'SullivanMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom Laura.Denby@ed.ac.uk Tamir.Chandra@ed.ac.uk.ORCID 0000-0002-7709-6595
Carolynn CairnsCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
James O'SullivanCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom Laura.Denby@ed.ac.uk Tamir.Chandra@ed.ac.uk.
Daniel J SimpsonInstitute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0002-8431-7384
Angela SalzanoInstitute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.
Katie ConnorCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Peng DingMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Duncan HumphriesMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Kevin StewartCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Oliver TeenanCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Riinu PiusCentre for Medical Informatics, University of Edinburgh, Edinburgh, United Kingdom.
Neil C HendersonMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Cécile BénézechCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Prakash RamachandranMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0001-5996-2413
David FerenbachMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0002-9202-1428
Jeremy HughesMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Tamir ChandraInstitute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom Laura.Denby@ed.ac.uk Tamir.Chandra@ed.ac.uk.
Laura DenbyCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom Laura.Denby@ed.ac.uk Tamir.Chandra@ed.ac.uk.ORCID 0000-0003-1277-708X
Queen's Medical Centre · GBThe Queen's Medical Research Institute · GBInstitute of Genetics and Cancer · GBUniversity of Edinburgh · GB

Funding

Medical Research Council MC_PC_15075Medical Research Council MR/M011542/1Medical Research Council MR/N008340/1Medical Research Council MR/S001743/1Wellcome Trust 103749
6 · The paper itself

Abstract

backgroundLittle is known about the roles of myeloid cell subsets in kidney injury and in the limited ability of the organ to repair itself. Characterizing these cells based only on surface markers using flow cytometry might not provide a full phenotypic picture. Defining these cells at the single-cell, transcriptomic level could reveal myeloid heterogeneity in the progression and regression of kidney disease.

methodsIntegrated droplet- and plate-based single-cell RNA sequencing were used in the murine, reversible, unilateral ureteric obstruction model to dissect the transcriptomic landscape at the single-cell level during renal injury and the resolution of fibrosis. Paired blood exchange tracked the fate of monocytes recruited to the injured kidney.

resultsA single-cell atlas of the kidney generated using transcriptomics revealed marked changes in the proportion and gene expression of renal cell types during injury and repair. Conventional flow cytometry markers would not have identified the 12 myeloid cell subsets. Monocytes recruited to the kidney early after injury rapidly adopt a proinflammatory, profibrotic phenotype that expresses

conclusionsComplementary technologies identified novel myeloid subtypes, based on transcriptomics in single cells, that represent therapeutic targets to inhibit progression or promote regression of kidney disease.

Indexed as

AnimalsDisease Models, AnimalDisease ProgressionKidney DiseasesMacrophagesMaleMiceMice, Inbred C57BLMyeloid CellsSequence Analysis, RNASingle-Cell AnalysisUreteral Obstructionfibrosiskidney diseasemyeloid cellsscRNA sequencing

Identifiers

PMID32978267
PMCPMC7790206
OpenAlexW3088826870

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.