Evidence map›Paper›PMID 22415011›Full record

ArticleMolecular medicine (Cambridge, Mass.)2012

Delayed administration of pyroglutamate helix B surface peptide (pHBSP), a novel nonerythropoietic analog of erythropoietin, attenuates acute kidney injury.

Nimesh S A Patel, Hannah L Kerr-Peterson, Michael Brines, Massimo Collino, Mara Rogazzo, Roberto Fantozzi, Elizabeth G Wood, Florence L Johnson, Muhammad M Yaqoob, Anthony Cerami and 1 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Targeting the innate repair receptor axisFrontiers in immunology · 2022
    Article
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Hypoxia: The Force that Drives Chronic Kidney Disease.Clinical medicine & research · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 3 countries.

Nimesh S A PatelQueen Mary University of London, Barts and The London School of Medicine and Dentistry, The William Harvey Research Institute, London, UK. n.s.patel@qmul.ac.uk
Hannah L Kerr-Peterson
Michael Brines
Massimo Collino
Mara Rogazzo
Roberto Fantozzi
Elizabeth G Wood
Florence L Johnson
Muhammad M Yaqoob
Anthony Cerami
Christoph Thiemermann
Queen Mary University of London · GBUniversity of Turin · ITAraim Pharmaceuticals (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In preclinical studies, erythropoietin (EPO) reduces ischemia-reperfusion-associated tissue injury (for example, stroke, myocardial infarction, acute kidney injury, hemorrhagic shock and liver ischemia). It has been proposed that the erythropoietic effects of EPO are mediated by the classic EPO receptor homodimer, whereas the tissue-protective effects are mediated by a hetero-complex between the EPO receptor monomer and the β-common receptor (termed "tissue-protective receptor"). Here, we investigate the effects of a novel, selective-ligand of the tissue-protective receptor (pyroglutamate helix B surface peptide [pHBSP]) in a rodent model of acute kidney injury/dysfunction. Administration of pHBSP (10 μg/kg intraperitoneally [i.p.] 6 h into reperfusion) or EPO (1,000 IU/kg i.p. 4 h into reperfusion) to rats subjected to 30 min ischemia and 48 h reperfusion resulted in significant attenuation of renal and tubular dysfunction. Both pHBSP and EPO enhanced the phosphorylation of Akt (activation) and glycogen synthase kinase 3β (inhibition) in the rat kidney after ischemia-reperfusion, resulting in prevention of the activation of nuclear factor-κB (reduction in nuclear translocation of p65). Interestingly, the phosphorylation of endothelial nitric oxide synthase was enhanced by EPO and, to a much lesser extent, by pHBSP, suggesting that the signaling pathways activated by EPO and pHBSP may not be identical.

Indexed as

Acute Kidney InjuryAnimalsClusterinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaKidney GlomerulusKidney TubulesMaleNF-kappa BNitric Oxide Synthase Type IIIOligopeptidesOsteopontinProtein TransportProto-Oncogene Proteins c-aktRatsRats, WistarcibinetideClusterinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratNF-kappa BNitric Oxide Synthase Type IIIOligopeptidesOsteopontinProto-Oncogene Proteins c-akt

Identifiers

PMID22415011
PMCPMC3388125
OpenAlexW2103797621

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.