Evidence map›Paper›PMID 24127583›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Differentiated kidney epithelial cells repair injured proximal tubule.

Tetsuro Kusaba, Matthew Lalli, Rafael Kramann, Akio Kobayashi, Benjamin D Humphreys

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 295 papers.

0numbers the graph read from it
0cells of the map it votes in
295citing papers in PubMed
17.3field-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

295 citing papers in PubMed, 475 citations in OpenAlex.

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  13. Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  14. Ketone Body Supplementation Exerts Renoprotective Effects Against Adenine-Induced Kidney Injury via OXCT1-Mediated Ketolysis in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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235 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Tetsuro KusabaRenal Division, Brigham and Women's Hospital, Boston, MA 02115.
Matthew Lalli
Rafael Kramann
Akio Kobayashi
Benjamin D Humphreys
Brigham and Women's Hospital · 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
Genetic Regulation of Nephron Progenitor Cells in the Mammalian KidneyR01DK094933 · NIDDK · UNIVERSITY OF WASHINGTON · PI KOBAYASHI, AKIO · 2013 to 2017
$1.9M
NIDDK NIH HHS DK088923NIDDK NIH HHS DK094933NIDDK NIH HHS R01 DK088923NIDDK NIH HHS R01 DK094933
6 · The paper itself

Abstract

Whether kidney proximal tubule harbors a scattered population of epithelial stem cells is a major unsolved question. Lineage-tracing studies, histologic characterization, and ex vivo functional analysis results conflict. To address this controversy, we analyzed the lineage and clonal behavior of fully differentiated proximal tubule epithelial cells after injury. A CreER(T2) cassette was knocked into the sodium-dependent inorganic phosphate transporter SLC34a1 locus, which is expressed only in differentiated proximal tubule. Tamoxifen-dependent recombination was absolutely specific to proximal tubule. Clonal analysis after injury and repair showed that the bulk of labeled cells proliferate after injury with increased clone size after severe compared with mild injury. Injury to labeled proximal tubule epithelia induced expression of CD24, CD133, vimentin, and kidney-injury molecule-1, markers of putative epithelial stem cells in the human kidney. Similar results were observed in cultured proximal tubules, in which labeled clones proliferated and expressed dedifferentiation and injury markers. When mice with completely labeled kidneys were subject to injury and repair there was no dilution of fate marker despite substantial proliferation, indicating that unlabeled progenitors do not contribute to kidney repair. During nephrogenesis and early kidney growth, single proximal tubule clones expanded, suggesting that differentiated cells also contribute to tubule elongation. These findings provide no evidence for an intratubular stem-cell population, but rather indicate that terminally differentiated epithelia reexpress apparent stem-cell markers during injury-induced dedifferentiation and repair.

Indexed as

Cell DifferentiationEpithelial CellsHumansKidneyKidney Tubules, ProximalRecombination, Genetic

Identifiers

PMID24127583
PMCPMC3910580
OpenAlexW2056109978

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.