Evidence map›Paper›PMID 20962739›Full record

ArticleKidney international2011

Inhibition of 20-HETE synthesis and action protects the kidney from ischemia/reperfusion injury.

Uwe Hoff, Ivo Lukitsch, Lyubov Chaykovska, Mechthild Ladwig, Cosima Arnold, Vijay L Manthati, T Florian Fuller, Wolfgang Schneider, Maik Gollasch, Dominik N Muller and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 75 citations in OpenAlex.

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  14. MRI Mapping of the Blood Oxygenation Sensitive Parameter TMethods in molecular biology (Clifton, N.J.) · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Uwe HoffNephrology and Intensive Care Medicine, Campus Virchow and Center for Cardiovascular Research, Charité Medical Faculty, Berlin, Germany.
Ivo Lukitsch
Lyubov Chaykovska
Mechthild Ladwig
Cosima Arnold
Vijay L Manthati
T Florian Fuller
Wolfgang Schneider
Maik Gollasch
Dominik N Muller
Bert Flemming
Erdmann Seeliger
Friedrich C Luft
John R Falck
Duska Dragun
Wolf-Hagen Schunck
Charité - Universitätsmedizin Berlin · DEMax Delbrück Center · DEThe University of Texas Southwestern Medical Center · US

Funding

TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
Novel Eicosanoids: Synthesis and FunctionR01GM031278 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI FALCK, JOHN R. · 1985 to 2012
$4.7M
NIDDK NIH HHS P01 DK038226NIGMS NIH HHS GM31278NIGMS NIH HHS R01 GM031278
6 · The paper itself

Abstract

20-Hydroxyeicosatetraenoic acid (20-HETE) production is increased in ischemic kidney tissue and may contribute to ischemia/reperfusion (I/R) injury by mediating vasoconstriction and inflammation. To test this hypothesis, uninephrectomized male Lewis rats were exposed to warm ischemia following pretreatment with either an inhibitor of 20-HETE synthesis (HET0016), an antagonist (20-hydroxyeicosa-6(Z),15(Z)-dienoic acid), an agonist (20-hydroxyeicosa-5(Z),14(Z)-dienoic acid), or vehicle via the renal artery and the kidneys were examined 2 days after reperfusion. Pretreatment with either the inhibitor or the antagonist attenuated I/R-induced renal dysfunction as shown by improved creatinine clearance and decreased plasma urea levels, compared to controls. The inhibitor and antagonist also markedly reduced tubular lesion scores, inflammatory cell infiltration, and tubular epithelial cell apoptosis. Administering the antagonist accelerated the recovery of medullary perfusion, as well as renal medullary and cortical re-oxygenation, during the early reperfusion phase. In contrast, the agonist did not improve renal injury and reversed the beneficial effect of the inhibitor. Thus, 20-HETE generation and its action mediated kidney injury due to I/R. Whether or not these effects are clinically important will need to be tested in appropriate human studies.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCreatineCytochrome P-450 Enzyme InhibitorsCytochrome P-450 Enzyme SystemCytochrome P450 Family 4Epithelial CellsHydroxyeicosatetraenoic AcidsKidney TubulesModels, AnimalRatsRats, Inbred LewReperfusion InjuryStatistics, NonparametricUrea20-hydroxy-5,8,11,14-eicosatetraenoic acid20-hydroxyeicosa-5(Z),14(Z)-dienoic acid20-hydroxyeicosa-6(Z),15(Z)-dienoic acidCreatineCyp4a1protein, ratCytochrome P-450 Enzyme InhibitorsCytochrome P-450 Enzyme SystemCytochrome P450 Family 4Hydroxyeicosatetraenoic AcidsUrea

Identifiers

PMID20962739
PMCPMC3813968
OpenAlexW2041744272

What OpenQuestion holds

Textmetadata
LicenceTDM
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.