Evidence map›Paper›PMID 25155054›Full record

ReviewNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2015

Who regenerates the kidney tubule?

Rafael Kramann, Tetsuro Kusaba, Benjamin D Humphreys

Open access · bronzeAbstract readReview
In one paragraph

Review in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
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  10. Retinoic acid receptor α activity in proximal tubules prevents kidney injury and fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Review
  12. Vitamin A and retinoid signaling in the kidneys.Pharmacology & therapeutics · 2023
    Review
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  15. Article
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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

3 authors at 2 institutions in 2 countries.

Rafael KramannBrigham and Women's Hospital, Boston, MA, USA Harvard Medical School, Boston, MA, USA Division of Nephrology, RWTH Aachen University, Aachen, Germany.
Tetsuro KusabaBrigham and Women's Hospital, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Benjamin D HumphreysBrigham and Women's Hospital, Boston, MA, USA Harvard Medical School, Boston, MA, USA Harvard Stem Cell Institute, Cambridge, MA, USA.
Harvard University · USHarvard Stem Cell Institute · US

Funding

Hedgehog Signaling in Kidney Homeostasis and RepairR01DK088923 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI HUMPHREYS, BENJAMIN D. · 2010 to 2014
$2.0M
Retinoic Acid in Myofibrolast Activation and Kidney FibrosisR01DK103050 · NIDDK · WASHINGTON UNIVERSITY · PI HUMPHREYS, BENJAMIN D. · 2014 to 2016
$701k
NIDDK NIH HHS NIH DK088923NIDDK NIH HHS R01 DK088923NIDDK NIH HHS R01 DK103050
6 · The paper itself

Abstract

The kidney possesses profound regenerative potential and in some cases can recover completely 'restitutio at integrum' following an acute kidney injury (AKI). Emerging evidence strongly suggests that sometimes repair is incomplete, however, and, in this situation, an episode of AKI leads to future chronic kidney disease (CKD). Understanding the tubular response after AKI will shed light on the relationship between incomplete repair and future risk of CKD. The first repair phase after AKI is characterized by robust proliferation of epithelial cells in the proximal tubule. The exact source of these proliferating cells has been a source of controversy for the last decade. While nearly everyone now agrees that reparative cells arise within the proximal tubule, there is disagreement about whether all surviving cells possess an equivalent repair capacity through dedifferentiation, or alternatively whether a pre-existing intratubular stem cell population [so-called scattered tubular cells (STC)] is responsible for repair. This review will summarize the evidence on both sides of this issue and will discuss very recent genetic fate-tracing data that strongly points against the existence of intratubular stem cells but rather indicates that terminally differentiated proximal tubule epithelial cells undergo dedifferentiation upon injury to replace lost neighboring tubular epithelial cells through proliferative self-duplication. This new evidence includes data clearly indicating that STC are not committed tubular stem cells but instead represent individual dedifferentiated tubular epithelial cells that transiently express putative stem cell markers.

Indexed as

Cell DifferentiationAcute Kidney InjuryHumansKidney TubulesRegenerationRenal Insufficiency, ChronicStem Cellsacute kidney injurydedifferentiationstem celltubular repair

Identifiers

PMID25155054
PMCPMC4438740
OpenAlexW2131658531

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.