Evidence mapPaperPMID 24489534Full record

ArticlePPAR research2013

PPARγ Agonist Rosiglitazone Suppresses Renal mPGES-1/PGE2 Pathway in db/db Mice.

Ying Sun, Zhanjun Jia, Gang Liu, Li Zhou, Mi Liu, Baoxue Yang, Tianxin Yang

Open access · goldAbstract read
In one paragraph

Article in PPAR research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. PGE2, Kidney Disease, and Cardiovascular Risk: Beyond Hypertension and Diabetes.Journal of the American Society of Nephrology : JASN · 2016
    Review
  11. Article
  12. Review
  13. 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

7 authors at 2 institutions in 2 countries.

Ying SunDepartment of Pharmacology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Haidian District, Beijing 100191, China ; Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA.
Zhanjun JiaDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA.
Gang LiuDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA.
Li ZhouDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA.
Mi LiuDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA.
Baoxue YangDepartment of Pharmacology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Tianxin YangDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA ; Division of Nephrology and Hypertension, University of Utah and Veterans Affairs Medical Center, 30N 1900E, RM 4C224, Salt Lake City, UT 84132, USA.
University of Utah · USPeking University · CN

Funding

NIDDK NIH HHS R01 DK079162
6 · The paper itself

Abstract

Evidence had shown the detrimental effect of prostaglandin (PG) E2 in diabetic nephropathy (DN) of STZ-induced type-1 diabetes but its role in the development of DN of type-2 diabetes remains uncertain. The present study was undertaken to investigate the regulation of PGE2 synthetic pathway and the interaction between peroxisome proliferator-activated receptor (PPAR) γ and PGE2 synthesis in the kidneys of db/db mice. Strikingly, urinary PGE2 was remarkably elevated in db/db mice paralleled with the increased protein expressions of COX-2 and mPGES-1. In contrast, the protein expressions of COX-1, mPGES-2, cPGES, and 15-hydroxyprostaglandin dehydrogenase (15-PGDH) were not altered. Following 1-week rosiglitazone (Rosi) therapy, urinary PGE2, but not other prostanoids, was reduced by 57% in parallel with significant reduction of mPGES-1 protein and EP4 mRNA expressions. By immunohistochemistry, mPGES-1 was significantly induced in the glomeruli of db/db mice, which was almost entirely abolished by Rosi. In line with the reduction of glomerular mPGES-1, the glomerular injury score showed a tendency of improvement after 1 week of Rosi therapy. Collectively, the present study demonstrated an inhibitory effect of PPAR γ activation on renal mPGES-1/PGE2/EP4 pathway in type-2 diabetes and suggested that mPGES-1 may potentially serve as a therapeutic target for treating type-2 diabetes-associated DN.

Identifiers

PMID24489534
PMCPMC3892750
OpenAlexW2164806144

What Socratic holds

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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 Socratic graph.