Evidence map›Paper›PMID 19861503›Full record

ArticleEndocrinology2009

Glucose promotes the production of interleukine-1beta and cyclooxygenase-2 in mesangial cells via enhanced (Pro)renin receptor expression.

Jiqian Huang, Helmy M Siragy

Abstract read
In one paragraph

Article in Endocrinology, 2009. 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
4.6field-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

51 citing papers in PubMed, 82 citations in OpenAlex.

  1. Renal tubular (pro)renin receptor deletion exacerbates kidney injury inAmerican journal of physiology. Renal physiology · 2025
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  5. Review
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  8. The HAmerican journal of physiology. Cell physiology · 2021
    Review
  9. Article
  10. Review
  11. The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Increased (pro)renin receptor expression in the subfornical organ of hypertensive humans.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  19. Prorenin receptor mediates inflammation in renal ischemia.Clinical and experimental pharmacology & physiology · 2018
    Article
  20. 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

2 authors at 1 institution in 1 country.

Jiqian HuangDepartment of Medicine, University of Virginia Health System, Charlottesville, Virginia 22908-1409, USA.
Helmy M Siragy
University of Virginia Health System · US

Funding

Prorenin Receptors Mediate Hypertension and Kidney Disease in DiabetesR01HL091535 · NHLBI · UNIVERSITY OF VIRGINIA · PI SIRAGY, HELMY M · 2008 to 2020
$5.1M
Renin receptor provoked renal inflammationR01DK078757 · NIDDK · UNIVERSITY OF VIRGINIA · PI SIRAGY, HELMY M · 2007 to 2016
$3.3M
NHLBI NIH HHS HL091535NHLBI NIH HHS R01 HL091535NIDDK NIH HHS DK-078757NIDDK NIH HHS R01 DK078757
6 · The paper itself

Abstract

(Pro)renin receptor (PRR) is present in renal glomeruli, and its expression is up-regulated in diabetes. Similarly, renal inflammation is increased in the presence of hyperglycemia. The linkage between PRR and renal inflammation is not well established. We hypothesized that glucose-induced up-regulation of PRR leads to increased production of the proinflammatory factors IL-1beta and cyclooxygenase-2 (COX-2). Studies were conducted in rat mesangial cells (RMCs) exposed to 30 mm D-glucose for 2 wk followed by PRR small interfering RNA knockdown, IL-1 receptor blockade with IL-1 receptor antagonist or angiotensin II type 1 receptor blockade with valsartan. The results showed that D-glucose treatment up-regulates prorenin, renin, angiotensin II, PRR, IL-1beta, and COX-2 mRNA and protein expression and increases phosphorylation of ERK1/2, c-Jun N-terminal kinase, c-Jun, and nuclear factor-kappaB (NF-kappaB) p65 (serine 276,468 and 536), respectively. PRR small interfering RNA attenuated PRR, IL-1beta, and COX-2 mRNA and protein expressions and significantly decreased angiotensin II production and phosphorylation of ERK1/2 and NF-kappaB p65 associated with high glucose exposure. Similarly, IL-1 receptor antagonist significantly reduced COX-2 mRNA and protein expression induced by high glucose. COX-2 inhibition reduced high-glucose-induced PRR expression. We conclude that glucose induces the up-regulation of PRR and its ligands prorenin and renin, leading to increased IL-1beta and COX-2 production via the angiotensin II-dependent pathway. It is also possible that PRR could enhance the production of these inflammatory cytokines through direct stimulation of ERK1/2-NF-kappaB signaling cascade.

Indexed as

Angiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsBlotting, WesternCells, CulturedCyclooxygenase 2Dose-Response Relationship, DrugGlucoseInterleukin-1betaMesangial CellsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProrenin ReceptorRatsReceptors, Cell SurfaceAngiotensin IIAngiotensin II Type 1 Receptor BlockersCyclooxygenase 2GlucoseInterleukin-1betaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Prorenin ReceptorReceptors, Cell SurfaceReninTetrazolesTranscription Factor RelAValineValsartan

Identifiers

PMID19861503
PMCPMC2795703
OpenAlexW2102806171

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.