Evidence map›Paper›PMID 23594675›Full record

ArticleKidney international2013

Erythropoietin attenuates acute kidney dysfunction in murine experimental sepsis by activation of the β-common receptor.

Sina M Coldewey, Areeg I Khan, Amar Kapoor, Massimo Collino, Mara Rogazzo, Michael Brines, Anthony Cerami, Peter Hall, Michael Sheaff, Julius E Kieswich and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
5.8field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Erythropoiesis-stimulating agents for preventing acute kidney injury.The Cochrane database of systematic reviews · 2024
    Pooled it
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  10. Targeting the innate repair receptor axisFrontiers in immunology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 4 countries.

Sina M ColdeweyThe William Harvey Research Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, London, UK. s.m.coldewey@qmul.ac.uk
Areeg I Khan
Amar Kapoor
Massimo Collino
Mara Rogazzo
Michael Brines
Anthony Cerami
Peter Hall
Michael Sheaff
Julius E Kieswich
Muhammed M Yaqoob
Nimesh S A Patel
Christoph Thiemermann
Queen Mary University of London · GBAraim Pharmaceuticals (United States) · USUniversity of Turin · ITAstraZeneca (United Kingdom) · GBBarts Health NHS Trust · GB

Funding

British Heart Foundation PG/11/30/28849Medical Research Council
6 · The paper itself

Abstract

The β-common receptor (βcR) plays a pivotal role in the nonhematopoietic tissue-protective effects of erythropoietin (EPO). Here we determined whether EPO reduces the acute kidney injury (AKI) caused by sepsis and whether this effect is mediated by the βcR. In young (2 months old) C57BL/6 wild-type and βcR knockout mice, lipopolysaccharide caused a significant increase in serum urea and creatinine, hence AKI. This AKI was not associated with any overt morphological alterations in the kidney and was attenuated by EPO given 1 h after lipopolysaccharide in wild-type but not in βcR knockout mice. In the kidneys of endotoxemic wild-type mice, EPO enhanced the phosphorylation of Akt, glycogen synthase kinase-3β, and endothelial nitric oxide synthase, and inhibited the activation of nuclear factor-κB. All these effects of EPO were lost in βcR knockout mice. Since sepsis is more severe in older animals or patients, we tested whether EPO was renoprotective in 8-month-old wild-type and βcR knockout mice that underwent cecal ligation and puncture. These older mice developed AKI at 24 h, which was attenuated by EPO treatment 1 h post cecal ligation and puncture in wild-type mice but not in βcR knockout mice. Thus, activation of the βcR by EPO is essential for the observed reduction in AKI in either endotoxemic young mice or older mice with polymicrobial sepsis, and for the activation of well-known signaling pathways by EPO.

Indexed as

Acute Kidney InjuryAnimalsCaspase 3CecumCytokine Receptor Common beta SubunitDisease Models, AnimalErythropoietinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHepatitis A Virus Cellular Receptor 1KidneyLigationLipopolysaccharidesMaleMembrane ProteinsMiceCaspase 3Cytokine Receptor Common beta SubunitErythropoietinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseHavcr1 protein, mouseHepatitis A Virus Cellular Receptor 1LipopolysaccharidesMembrane ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID23594675
OpenAlexW2092057596

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.