Evidence map›Paper›PMID 23980070›Full record

ArticleHypertension (Dallas, Tex. : 1979)2013

Orally active epoxyeicosatrienoic acid analog attenuates kidney injury in hypertensive Dahl salt-sensitive rat.

Md Abdul Hye Khan, Jan Neckár, Vijay Manthati, Ramu Errabelli, Tengis S Pavlov, Alexander Staruschenko, John R Falck, John D Imig

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Inflammatory macrophages in the kidney contribute to salt-sensitive hypertension.American journal of physiology. Renal physiology · 2020
    Review
  11. Epoxyeicosanoids in hypertension.Physiological research · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

8 authors at 3 institutions in 2 countries.

Md Abdul Hye KhanMedical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. jdimig@mcw.edu.
Jan Neckár
Vijay Manthati
Ramu Errabelli
Tengis S Pavlov
Alexander Staruschenko
John R Falck
John D Imig
Czech Academy of Sciences, Institute of Physiology · CZMedical College of Wisconsin · USCzech Academy of Sciences · CZ

Funding

TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR031973 · NCRR · MEDICAL COLLEGE OF WISCONSIN · PI SHAKER, REZA NONE · 2010 to 2011
$7.9M
Novel Eicosanoids: Synthesis and FunctionR01GM031278 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI FALCK, JOHN R. · 1985 to 2012
$4.7M
Mechanisms and relevance of ENaC regulation by EGF and Rac1R01HL108880 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STARUSCHENKO, ALEXANDER · 2012 to 2016
$1.9M
Regulation of ENaC in salt-sensitive hypertension via inflammation-induced ROS prK99HL116603 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PAVLOV, TENGIS S · 2013 to 2014
$180k
NCRR NIH HHS UL1 RR031973NCRR NIH HHS UL1RR031973NHLBI NIH HHS K99 HL116603NHLBI NIH HHS R01 HL108880NIDDK NIH HHS DK38226NIDDK NIH HHS P01 DK038226NIGMS NIH HHS GM31278NIGMS NIH HHS R01 GM031278
6 · The paper itself

Abstract

Salt-sensitive hypertension leads to kidney injury. The Dahl salt-sensitive hypertensive rat (Dahl SS) is a model of salt-sensitive hypertension and progressive kidney injury. The current set of experimental studies evaluated the kidney protective potential of a novel epoxyeicosatrienoic acid analog (EET-B) in Dahl SS hypertension. Dahl SS rats receiving high-salt diet were treated with EET-B (10 mg/kg per day) or vehicle in drinking water for 14 days. Urine, plasma, and tissue samples were collected at the end of the treatment protocol to assess kidney injury, oxidative stress, inflammation, and endoplasmic reticulum stress. EET-B treatment in Dahl SS rats markedly reduced urinary albumin and nephrin excretion by 60% to 75% along with 30% to 60% reductions in glomerular injury, intratubular cast formation, and kidney fibrosis without affecting blood pressure. In Dahl SS rats, EET-B treatment further caused marked reduction in oxidative stress with 25% to 30% decrease in kidney malondialdehyde content along with 42% increase of nitrate/nitrite and a 40% reduction of 8-isoprostane. EET-B treatment reduced urinary monocyte chemoattractant protein-1 by 50% along with a 40% reduction in macrophage infiltration in the kidney. Treatment with EET-B markedly reduced renal endoplasmic reticulum stress in Dahl SS rats with reduction in the kidney mRNA expressions and immunoreactivity of glucose regulatory protein 78 and C/EBP homologous protein. In summary, these experimental findings reveal that EET-B provides kidney protection in Dahl SS rats by reducing oxidative stress, inflammation, and endoplasmic reticulum stress, and this protection was independent of reducing blood pressure.

Indexed as

AnimalsBlood PressureEicosanoidsEndoplasmic Reticulum StressHumansHuman Umbilical Vein Endothelial CellsHypertensionInflammationKidneyKidney DiseasesOxidative StressRatsRats, Inbred DahlSodium Chloride, DietaryEicosanoidsSodium Chloride, Dietaryarachidonate epoxygenaseglomerular necrosishypertensioninflammationoxidative stress

Identifiers

PMID23980070
PMCPMC3872985
OpenAlexW2136463259

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.