Evidence map›Paper›PMID 33670614›Full record

ArticleJournal of clinical medicine2021

Agonism of Prostaglandin E2 Receptor 4 Ameliorates Tubulointerstitial Injury in Nephrotoxic Serum Nephritis in Mice.

Ida Aringer, Katharina Artinger, Corinna Schabhüttl, Thomas Bärnthaler, Agnes A Mooslechner, Andrijana Kirsch, Marion Pollheimer, Philipp Eller, Alexander R Rosenkranz, Akos Heinemann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Prostaglandin EEXCLI journal · 2025
    Review
  2. Single hormone or synthetic agonist induces GProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Prostanoid receptors in hyperfiltration-mediated glomerular injury: Novel agonists and antagonists reveal opposing roles for EP2 and EP4 receptors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  4. 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

11 authors at 1 institution in 1 country.

Ida AringerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.
Katharina ArtingerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.
Corinna SchabhüttlClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.
Thomas BärnthalerOtto Loewi Research Center, Division of Pharmacology, Medical University of Graz, BioTechMed Graz, 8036 Graz, Austria.
Agnes A MooslechnerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.
Andrijana KirschClinical Department of Phoniatrics, Medical University of Graz, 8036 Graz, Austria.ORCID 0000-0002-6623-0234
Marion PollheimerInstitute of Pathology, Medical University of Graz, 8036 Graz, Austria.
Philipp EllerIntensive Care Unit, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.ORCID 0000-0001-5537-3646
Alexander R RosenkranzClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.
Akos HeinemannOtto Loewi Research Center, Division of Pharmacology, Medical University of Graz, BioTechMed Graz, 8036 Graz, Austria.ORCID 0000-0002-8554-2372
Kathrin EllerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.ORCID 0000-0002-6214-5008
Medical University of Graz · AT

Funding

Austrian Science Fund FWF J 4547
6 · The paper itself

Abstract

Selectively targeting the E-type prostanoid receptor 4 (EP4) might be a new therapeutic option in the treatment of glomerulonephritis (GN), since the EP4 receptor is expressed on different immune cells, resident kidney cells, and endothelial cells, which are all involved in the pathogenesis of immune-complex GN. This study aimed to evaluate the therapeutic potential and to understand the mode of action of EP4 agonist in immune-complex GN using the murine model of nephrotoxic serum nephritis (NTS). In vivo, NTS mice were treated two times daily with two different doses of an EP4 agonist ONO AE1-329 or vehicle for 14 days total. The effect of PGE2 and EP4 agonism and antagonism was tested on murine distal convoluted tubular epithelial cells (DCT) in vitro. In vivo, the higher dose of the EP4 agonist led to an improved NTS phenotype, including a reduced tubular injury score and reduced neutrophil gelatinase-associated lipocalin (NGAL) and blood urea nitrogen (BUN) levels. EP4 agonist treatment caused decreased CD4

Indexed as

EP4 receptorglomerulonephritislipid mediatorNTSPGE2

Identifiers

PMID33670614
PMCPMC7922874
OpenAlexW3130593829

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.