Evidence map›Paper›PMID 26911791›Full record

ArticleScientific reports2016

The Synthetic Tie2 Agonist Peptide Vasculotide Protects Renal Vascular Barrier Function In Experimental Acute Kidney Injury.

Eva Rübig, Jörg Stypmann, Paul Van Slyke, Daniel J Dumont, Tilmann Spieker, Konrad Buscher, Stefan Reuter, Tobias Goerge, Hermann Pavenstädt, Philipp Kümpers

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  8. The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023
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  16. Review
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  18. Article
  19. Angiopoietins as Potential Targets in Management of Retinal Disease.Clinical ophthalmology (Auckland, N.Z.) · 2021
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Eva RübigDepartment of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
Jörg StypmannDepartment of Cardiology, University Hospital Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
Paul Van SlykeVasomune Therapeutics, 661 University Avenue Suite 465, Toronto, Ontario, Canada.
Daniel J DumontMolecular and Cellular Biology Research, Sunnybrook Research Institute, and Department of Medical Biophysics, University of Toronto, Ontario, Canada.
Tilmann SpiekerInstitute of Pathology at St Franziskus Hospital Münster, Hohenzollernring 64, 48145 Münster, Germany.
Konrad BuscherDepartment of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
Stefan ReuterDepartment of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
Tobias GoergeDepartment of Dermatology, University Hospital Münster, Von-Esmarch-Straße 58, 48149 Münster, Germany.
Hermann PavenstädtDepartment of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
Philipp KümpersDepartment of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
University Hospital Münster · DESt. Franziskus Hospital · DESunnybrook Health Science Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microvascular barrier dysfunction plays a major role in the pathophysiology of acute kidney injury (AKI). Angiopoietin-1, the natural agonist ligand for the endothelial-specific Tie2 receptor, is a non-redundant endothelial survival and vascular stabilization factor. Here we evaluate the efficacy of a polyethylene glycol-clustered Tie2 agonist peptide, vasculotide (VT), to protect against endothelial-cell activation with subsequent microvascular dysfunction in a murine model of ischemic AKI. Renal ischemia reperfusion injury (IRI) was induced by clamping of the renal arteries for 35 minutes. Mice were treated with VT or PEGylated cysteine before IRI. Sham-operated animals served as time-matched controls. Treatment with VT significantly reduced transcapillary albumin flux and renal tissue edema after IRI. The protective effects of VT were associated with activation of Tie2 and stabilization of its downstream effector, VE-cadherin in renal vasculature. VT abolished the decline in renal tissue blood flow, attenuated the increase of serum creatinine and blood urea nitrogen after IRI, improved recovery of renal function and markedly reduced mortality compared to PEG [HR 0.14 (95% CI 0.05-0.78) P < 0.05]. VT is inexpensive to produce, chemically stable and unrelated to any Tie2 ligands. Thus, VT may represent a novel therapy to prevent AKI in patients.

Indexed as

Acute Kidney InjuryAlbuminsAngiopoietin-1AnimalsBiomimetic MaterialsCapillary PermeabilityCreatinineKidneyMaleMiceMice, Inbred C57BLModels, AnimalPeptide FragmentsReceptor, TIE-2Reperfusion InjuryAlbuminsAngiopoietin-1CreatininePeptide FragmentsReceptor, TIE-2Tek protein, mouseVasculotide

Identifiers

PMID26911791
PMCPMC4766468
OpenAlexW2412336661

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.