Evidence map›Paper›PMID 32111728›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

The Integrated RNA Landscape of Renal Preconditioning against Ischemia-Reperfusion Injury.

Marc Johnsen, Torsten Kubacki, Assa Yeroslaviz, Martin Richard Späth, Jannis Mörsdorf, Heike Göbel, Katrin Bohl, Michael Ignarski, Caroline Meharg, Bianca Habermann and 6 more

Erratum issuedOpen access · greenAbstract 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. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 4 countries.

Marc JohnsenDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Torsten KubackiDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Assa YeroslavizMax Planck Institute of Biochemistry, Martinsried, Germany.ORCID 0000-0001-9638-4026
Martin Richard SpäthDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Jannis MörsdorfDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Heike GöbelInstitute for Pathology, Diagnostic and Experimental Nephropathology Unit.
Katrin BohlDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Michael IgnarskiDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Caroline MehargInstitute for Global Food Security, Queen's University Belfast, Belfast, Northern Ireland, United Kingdom; and.
Bianca HabermannDevelopment Biology Institute of Marseille, Aix-Marseille University, CNRS, Marseille, France.
Janine AltmüllerCologne Center for Genomics, and.
Andreas BeyerInstitute for Pathology, Diagnostic and Experimental Nephropathology Unit.
Thomas BenzingDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Bernhard SchermerDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Volker BurstDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; roman-ulrich.mueller@uk-koeln.de volker.burst@uk-koeln.de.
Roman-Ulrich MüllerDepartment II of Internal Medicine and Center for Molecular Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; roman-ulrich.mueller@uk-koeln.de volker.burst@uk-koeln.de.ORCID 0000-0001-6910-0745
University of Cologne · DEArkana Laboratories · USCentre National de la Recherche Scientifique · FRMax Planck Institute of Biochemistry · DEQueen's University Belfast · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough AKI lacks effective therapeutic approaches, preventive strategies using preconditioning protocols, including caloric restriction and hypoxic preconditioning, have been shown to prevent injury in animal models. A better understanding of the molecular mechanisms that underlie the enhanced resistance to AKI conferred by such approaches is needed to facilitate clinical use. We hypothesized that these preconditioning strategies use similar pathways to augment cellular stress resistance.

methodsTo identify genes and pathways shared by caloric restriction and hypoxic preconditioning, we used RNA-sequencing transcriptome profiling to compare the transcriptional response with both modes of preconditioning in mice before and after renal ischemia-reperfusion injury.

resultsThe gene expression signatures induced by both preconditioning strategies involve distinct common genes and pathways that overlap significantly with the transcriptional changes observed after ischemia-reperfusion injury. These changes primarily affect oxidation-reduction processes and have a major effect on mitochondrial processes. We found that 16 of the genes differentially regulated by both modes of preconditioning were strongly correlated with clinical outcome; most of these genes had not previously been directly linked to AKI.

conclusionsThis comparative analysis of the gene expression signatures in preconditioning strategies shows overlapping patterns in caloric restriction and hypoxic preconditioning, pointing toward common molecular mechanisms. Our analysis identified a limited set of target genes not previously known to be associated with AKI; further study of their potential to provide the basis for novel preventive strategies is warranted. To allow for optimal interactive usability of the data by the kidney research community, we provide an online interface for user-defined interrogation of the gene expression datasets (http://shiny.cecad.uni-koeln.de:3838/IRaP/).

Indexed as

Caloric RestrictionHypoxiaAcute Kidney InjuryAnimalsGene Expression ProfilingIschemic PreconditioningMaleMiceMice, Inbred C57BLReperfusion InjuryRNA, MessengerRNA, Messengeracute renal failurecaloric restrictionhypoxiaischemia-reperfusionpreconditioningtranscriptional profiling

Identifiers

PMID32111728
PMCPMC7191926
OpenAlexW3007767068

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.