Evidence map›Paper›PMID 22414856›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2012

Attenuation of cisplatin-induced renal injury by inhibition of soluble epoxide hydrolase involves nuclear factor κB signaling.

Yingmei Liu, Heather K Webb, Hisayo Fukushima, Janine Micheli, Svetlana Markova, Jean L Olson, Deanna L Kroetz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  12. Review
  13. Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3β signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  14. Orally Active Epoxyeicosatrienoic Acid Analogs.Journal of cardiovascular pharmacology · 2017
    Review
  15. Effect of Cytochrome P450 Metabolites of Arachidonic Acid in Nephrology.Journal of the American Society of Nephrology : JASN · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

7 authors at 1 institution in 1 country.

Yingmei LiuDepartment of Bioengineering, University of California, San Francisco, San Francisco, CA 94158, USA.
Heather K Webb
Hisayo Fukushima
Janine Micheli
Svetlana Markova
Jean L Olson
Deanna L Kroetz
University of California, San Francisco · US

Funding

PHARMACEUTICAL SCIENCES AND PHARMACOGENOMICST32GM007175 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AHITUV, NADAV, KROETZ, DEANNA L · 1985 to 2021
$7.1M
Mechanisms of Renoprotection by Soluble Epoxide Hydrolase InhibitionR01DK084147 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KROETZ, DEANNA L · 2010 to 2014
$1.9M
NIDDK NIH HHS DK084147NIDDK NIH HHS R01 DK084147NIGMS NIH HHS T32 GM007175NIGMS NIH HHS T32-GM007175
6 · The paper itself

Abstract

Acute kidney injury is associated with a significant inflammatory response that has been the target of renoprotection strategies. Epoxyeicosatrienoic acids (EETs) are anti-inflammatory cytochrome P450-derived eicosanoids that are abundantly produced in the kidney and metabolized by soluble epoxide hydrolase (sEH; Ephx2) to less active dihydroxyeicosatrienoic acids. Genetic disruption of Ephx2 and chemical inhibition of sEH were used to test whether the anti-inflammatory effects of EETs, and other lipid epoxide substrates of sEH, afford protection against cisplatin-induced nephrotoxicity. EET hydrolysis was significantly reduced in Ephx2(-/-) mice and was associated with an attenuation of cisplatin-induced increases in serum urea nitrogen and creatinine levels. Histological evidence of renal tubular damage and neutrophil infiltration was also reduced in the Ephx2(-/-) mice. Likewise, cisplatin had no effect on renal function, neutrophil infiltration, or tubular structure and integrity in mice treated with the potent sEH inhibitor 1-adamantan-1-yl-3-(1-methylsulfonyl-piperidin-4-yl-urea) (AR9273). Consistent with the ability of EETs to interfere with nuclear factor-κB (NF-κB) signaling, the observed renoprotection was associated with attenuation of renal NF-κB activity and corresponding decreases in the expression of tumor necrosis factor (TNF) α, TNF receptor (TNFR) 1, TNFR2, and intercellular adhesive molecule-1 before the detection of tubular injury. These data suggest that EETs or other fatty acid epoxides can attenuate cisplatin-induced kidney injury and sEH inhibition is a novel renoprotective strategy.

Indexed as

8,11,14-Eicosatrienoic AcidAcute Kidney InjuryAdamantaneAnimalsAntineoplastic AgentsBlood Urea NitrogenCisplatinCreatinineEnzyme InhibitorsEpoxide HydrolasesIntercellular Adhesion Molecule-1MaleMiceMice, Inbred C57BLMice, KnockoutNF-kappa B8,11,14-Eicosatrienoic AcidAdamantaneAntineoplastic AgentsCisplatinCreatinineEnzyme InhibitorsEphx2 protein, mouseEpoxide HydrolasesIntercellular Adhesion Molecule-1NF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID22414856
PMCPMC3362876
OpenAlexW2147993286

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.