Evidence map›Paper›PMID 30202007›Full record

ArticleNature communications2018

CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury.

Toma A Yakulov, Abhijeet P Todkar, Krasimir Slanchev, Johannes Wiegel, Alexandra Bona, Martin Groß, Alexander Scholz, Isabell Hess, Anne Wurditsch, Florian Grahammer and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

38 citing papers in PubMed, 49 citations in OpenAlex.

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  11. Journal of cardiovascular development and disease · 2023
    Article
  12. Transgenic IDH2Oncogene · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 2 countries.

Toma A YakulovRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.ORCID http://orcid.org/0000-0002-3160-0944
Abhijeet P TodkarRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.ORCID http://orcid.org/0000-0002-8699-0425
Krasimir SlanchevRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Johannes WiegelRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.ORCID http://orcid.org/0000-0002-4006-9307
Alexandra BonaRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Martin GroßRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Alexander ScholzRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Isabell HessRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Anne WurditschRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Florian GrahammerRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Tobias B HuberRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Virginie LecaudeyFaculty of Biology, University of Freiburg, Schaenzlestrasse 1, 79104, Freiburg, Germany.
Tillmann BorkRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Jochen HochreinInstitute of Molecular Medicine and Cell Research, Faculty of Medicine, University of Freiburg, Stefan-Meier Strasse 17, 79104, Freiburg, Germany.
Melanie BoerriesInstitute of Molecular Medicine and Cell Research, Faculty of Medicine, University of Freiburg, Stefan-Meier Strasse 17, 79104, Freiburg, Germany.
Justine LeendersCenter for Interdisciplinary Research on Medicines (CIRM), Metabolomics Group, University of Liège, Avenue Hippocrate 15, 4000 Liège, Belgium.
Pascal de TullioCenter for Interdisciplinary Research on Medicines (CIRM), Metabolomics Group, University of Liège, Avenue Hippocrate 15, 4000 Liège, Belgium.
François JouretDivision of Nephrology, University of Liège Hospital, 4000 Liège, Belgium.ORCID http://orcid.org/0000-0003-2547-6593
Albrecht Kramer-ZuckerRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Gerd WalzRenal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany. gerd.walz@uniklinik-freiburg.de.ORCID http://orcid.org/0000-0002-4950-9946
University of Freiburg · DEUniversity of Liège · BEUniversität Hamburg · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos. Gene expression profiles between these two developmental stages identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAnimals, Genetically ModifiedCell MovementChemokine CXCL12Energy MetabolismGene DeletionGene Expression ProfilingGlycolysisHomeostasisKidneyKidney DiseasesMaleMiceMice, Inbred C57BLProto-Oncogene ProteinsChemokine CXCL12cxcl12a protein, zebrafishmycn protein, zebrafishProto-Oncogene ProteinsTretinoinZebrafish Proteins

Identifiers

PMID30202007
PMCPMC6131511
OpenAlexW2891706128

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.