Evidence map›Paper›PMID 33115917›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Single-Cell Profiling of AKI in a Murine Model Reveals Novel Transcriptional Signatures, Profibrotic Phenotype, and Epithelial-to-Stromal Crosstalk.

Valeria Rudman-Melnick, Mike Adam, Andrew Potter, Saagar M Chokshi, Qing Ma, Keri A Drake, Meredith P Schuh, J Matthew Kofron, Prasad Devarajan, S Steven Potter

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 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
11.8field-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

113 citing papers in PubMed, 203 citations in OpenAlex.

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  9. iScience · 2026
    Article
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  12. Review
  13. Article
  14. Article
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  16. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Valeria Rudman-MelnickDivision of Developmental Biology, Cincinnati Children's Medical Center, Cincinnati, Ohio.
Mike AdamDivision of Developmental Biology, Cincinnati Children's Medical Center, Cincinnati, Ohio.
Andrew PotterDivision of Developmental Biology, Cincinnati Children's Medical Center, Cincinnati, Ohio.
Saagar M ChokshiDivision of Nephrology and Hypertension, Cincinnati Children's Medical Center, Cincinnati, Ohio.
Qing MaDivision of Nephrology and Hypertension, Cincinnati Children's Medical Center, Cincinnati, Ohio.
Keri A DrakeDivision of Pediatric Nephrology, University of Texas Southwestern Medical Center, Dallas, Texas.
Meredith P SchuhDivision of Nephrology and Hypertension, Cincinnati Children's Medical Center, Cincinnati, Ohio.ORCID 0000-0001-7854-8138
J Matthew KofronDivision of Developmental Biology, Cincinnati Children's Medical Center, Cincinnati, Ohio.
Prasad DevarajanDivision of Nephrology and Hypertension, Cincinnati Children's Medical Center, Cincinnati, Ohio.
S Steven PotterDivision of Developmental Biology, Cincinnati Children's Medical Center, Cincinnati, Ohio Steve.Potter@cchmc.org.
Cincinnati Children's Hospital Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Proteomics CoreP50DK096418 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI DEVARAJAN, PRASAD · 2012 to 2021
$8.4M
Hox Genes & Lineage InfidelityR01DK120842 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PARK, JOO-SEOP · 2019 to 2023
$2.5M
NIDDK NIH HHS P50 DK096418NIDDK NIH HHS R01 DK120842
6 · The paper itself

Abstract

backgroundCurrent management of AKI, a potentially fatal disorder that can also initiate or exacerbate CKD, is merely supportive. Therefore, deeper understanding of the molecular pathways perturbed in AKI is needed to identify targets with potential to lead to improved treatment.

methodsWe performed single-cell RNA sequencing (scRNA-seq) with the clinically relevant unilateral ischemia-reperfusion murine model of AKI at days 1, 2, 4, 7, 11, and 14 after AKI onset. Using real-time quantitative PCR, immunofluorescence, Western blotting, and both chromogenic and single-molecule

resultsOur findings show the time course of changing gene expression patterns for multiple AKI stages and all renal cell types. We observed elevated expression of crucial injury response factors-including kidney injury molecule-1 (Kim1), lipocalin 2 (Lcn2), and keratin 8 (Krt8)-and of several novel genes (

conclusionsThe scRNA-seq, comprehensive, cell-specific profiles provide a valuable resource for examining molecular pathways that are perturbed in AKI. The results fully define AKI-associated dedifferentiation programs, potential pathologic ligand-receptor crosstalk, novel genes, and the improved injury response in younger mice, and highlight potential targets of kidney injury.

Indexed as

Acute Kidney InjuryAnimalsCell CommunicationDisease Models, AnimalEpithelial CellsKidney Tubules, ProximalMaleMicePhenotypeReal-Time Polymerase Chain ReactionReperfusion InjurySequence Analysis, RNAStromal Cellsacute kidney injurycellular crosstalkrenal developmental genessingle-cell

Identifiers

PMID33115917
PMCPMC7790221
OpenAlexW3097868566

What Socratic 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 Socratic graph.