Evidence map›Paper›PMID 25377915›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Pharmacological inhibition of soluble epoxide hydrolase prevents renal interstitial fibrogenesis in obstructive nephropathy.

Jinu Kim, Sang Pil Yoon, Myron L Toews, John D Imig, Sung Hee Hwang, Bruce D Hammock, Babu J Padanilam

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.5field-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

51 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Soluble Epoxide Hydrolase Inhibitors Improve Cornea Alkali Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. THE EFFECT OF COMPOUND DM509 ON KIDNEY FIBROSIS IN THE CONDITIONS OF THE EXPERIMENTAL MODEL.Visnyk Kyivs'koho natsional'noho universytetu imeni Tarasa Shevchenka. Biolohiia · 2020
    Article
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 4 institutions in 2 countries.

Jinu KimDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; Department of Anatomy, Jeju National University School of Medicine, Jeju, Republic of Korea; Department of Biomedicine and Drug Development, Jeju National University, Jeju, Republic of Korea;
Sang Pil YoonDepartment of Anatomy, Jeju National University School of Medicine, Jeju, Republic of Korea;
Myron L ToewsDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska;
John D ImigDepartment of Pharmacology and Toxicology and Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin;
Sung Hee HwangDepartment of Entomology and Comprehensive Cancer Center, University of California, Davis, California; and.
Bruce D HammockDepartment of Entomology and Comprehensive Cancer Center, University of California, Davis, California; and.
Babu J PadanilamDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; Department of Internal Medicine, Section of Nephrology, University of Nebraska Medical Center, Omaha, Nebraska bpadanilam@unmc.edu.
Jeju National University · KRUniversity of California, Davis · USUniversity of Nebraska Medical Center · USMedical College of Wisconsin · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
Regulation of Apoptosis in Renal IschemiaR01DK083291 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PADANILAM, BABU JOSEPH · 2010 to 2013
$1.3M
NIDDK NIH HHS DK-083291NIDDK NIH HHS DK-38226NIDDK NIH HHS R01 DK083291NIEHS NIH HHS P42 ES004699NIEHS NIH HHS P42-ES-04699NIEHS NIH HHS R01 ES002710NIEHS NIH HHS R01-ES-02710
6 · The paper itself

Abstract

Treating chronic kidney disease (CKD) has been challenging because of its pathogenic complexity. Epoxyeicosatrienoic acids (EETs) are cytochrome P-450-dependent derivatives of arachidonic acid with antihypertensive, anti-inflammatory, and profibrinolytic functions. We recently reported that genetic ablation of soluble epoxide hydrolase (sEH), an enzyme that converts EETs to less active dihydroxyeicosatrienoic acids, prevents renal tubulointerstitial fibrosis and inflammation in experimental mouse models of CKD. Here, we tested the hypothesis that pharmacological inhibition of sEH after unilateral ureteral obstruction (UUO) would attenuate tubulointerstitial fibrosis and inflammation in mouse kidneys and may provide a novel approach to manage the progression of CKD. Inhibition of sEH enhanced levels of EET regioisomers and abolished tubulointerstitial fibrosis, as demonstrated by reduced collagen deposition and myofibroblast formation after UUO. The inflammatory response was also attenuated, as demonstrated by decreased influx of neutrophils and macrophages and decreased expression of inflammatory cytokines keratinocyte chemoattractant, macrophage inflammatory protein-2, monocyte chemotactic protein-1, TNF-α, and ICAM-1 in kidneys after UUO. UUO upregulated transforming growth factor-β1/Smad3 signaling and induced NF-κB activation, oxidative stress, tubular injury, and apoptosis; in contrast, it downregulated antifibrotic factors, including peroxisome proliferator-activated receptor (PPAR) isoforms, especially PPAR-γ. sEH inhibition mitigated the aforementioned malevolent effects in UUO kidneys. These data demonstrate that pharmacological inhibition of sEH promotes anti-inflammatory and fibroprotective effects in UUO kidneys by preventing tubular injury, downregulation of NF-κB, transforming growth factor-β1/Smad3, and inflammatory signaling pathways, and activation of PPAR isoforms. Our data suggest the potential use of sEH inhibitors in treating fibrogenesis in the UUO model of CKD.

Indexed as

AnimalsArachidonic AcidsBenzoatesBlood PressureCell DeathDrug Evaluation, PreclinicalEpoxide HydrolasesMaleMice, Inbred C57BLNephrosclerosisOxidative StressPeroxisome Proliferator-Activated ReceptorsPhenylurea CompoundsRenal CirculationRenal Insufficiency, ChronicUreteral Obstruction4-(4-(3-(4-trifluoromethoxy-phenyl)ureido)cyclohexyloxy)benzoic acidArachidonic AcidsBenzoatesEpoxide HydrolasesPeroxisome Proliferator-Activated ReceptorsPhenylurea Compoundschronic kidney diseaseepoxyeicosatrienoic acidperoxisome proliferator-activated receptorsoluble epoxide hydrolasetrans-4-{4-[3-(4-trifluoromethoxyphenyl)ureido]cyclohexyloxy}benzoic acid

Identifiers

PMID25377915
PMCPMC4338924
OpenAlexW2117468217

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.