Evidence map›Paper›PMID 18535668›Full record

ArticleThe Journal of clinical investigation2008

Succinate receptor GPR91 provides a direct link between high glucose levels and renin release in murine and rabbit kidney.

Ildikó Toma, Jung Julie Kang, Arnold Sipos, Sarah Vargas, Eric Bansal, Fiona Hanner, Elliott Meer, János Peti-Peterdi

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

174 citing papers in PubMed, 321 citations in OpenAlex.

  1. Trial
  2. International journal of molecular sciences · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Mechanisms Involved in Pathological Succinate-Mediated Signaling.International journal of molecular sciences · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Vascular changes and their implications in lipedema.Frontiers in cell and developmental biology · 2026
    Review
  12. Review
  13. Review
  14. Emerging roles of the metabolite succinate in bone-related diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  15. World journal of gastroenterology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

114 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Ildikó TomaDepartment of Physiology and Biophysics, University of Southern California, Los Angeles, California 90033, USA.
Jung Julie Kang
Arnold Sipos
Sarah Vargas
Eric Bansal
Fiona Hanner
Elliott Meer
János Peti-Peterdi
University of Southern California · US

Funding

Multiphoton Imaging of the Juxtaglomerular ApparatusR01DK064324 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JANOS PETI-PETERDI · 2004 to 2026
$8.4M
Regulation of Renal Function by PGE2 and PGF2a ReceptorsR01DK037097 · NIDDK · VANDERBILT UNIVERSITY · PI BREYER, RICHARD M. · 1986 to 2011
$3.9M
Renin activation in early diabetesR01DK074754 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI PETI-PETERDI, JANOS · 2007 to 2009
$724k
NIDDK NIH HHS DK37097NIDDK NIH HHS DK64324NIDDK NIH HHS DK74754NIDDK NIH HHS R01 DK037097NIDDK NIH HHS R01 DK064324NIDDK NIH HHS R01 DK074754
6 · The paper itself

Abstract

Diabetes mellitus is the most common and rapidly growing cause of end-stage renal disease in developed countries. A classic hallmark of early diabetes mellitus includes activation of the renin-angiotensin system (RAS), which may lead to hypertension and renal tissue injury, but the mechanism of RAS activation is elusive. Here we identified a paracrine signaling pathway in the kidney in which high levels of glucose directly triggered the release of the prohypertensive hormone renin. The signaling cascade involved the local accumulation of succinate and activation of the kidney-specific G protein-coupled metabolic receptor, GPR91, in the glomerular endothelium as observed in rat, mouse, and rabbit kidney sections. Elements of signal transduction included endothelial Ca2+, the production of NO and prostaglandin (PGE2), and their paracrine actions on adjacent renin-producing cells. This GPR91 signaling cascade may serve to modulate kidney function and help remove metabolic waste products through renal hyperfiltration, and it could also link metabolic diseases, such as diabetes, or metabolic syndrome with RAS overactivation, systemic hypertension, and organ injury.

Indexed as

AnimalsCalcium SignalingCitratesDiabetes Mellitus, ExperimentalDinoprostoneEndothelial CellsFemaleGlucoseHyperglycemiaJuxtaglomerular ApparatusKidneyMaleMalonatesMiceMice, Inbred C57BLMice, KnockoutCitratesDinoprostonefluorocitrateGlucoseGPR91 protein, mouseMalonatesmalonic acidNitric OxideReceptors, G-Protein-CoupledReninSuccinic Acid

Identifiers

PMID18535668
PMCPMC2413183
OpenAlexW2125951881

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.