Evidence map›Paper›PMID 22203739›Full record

ArticleHypertension (Dallas, Tex. : 1979)2012

Sodium depletion enhances renal expression of (pro)renin receptor via cyclic GMP-protein kinase G signaling pathway.

Jiqian Huang, Helmy M Siragy

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019
    Review
  7. Soluble (pro)renin receptor as a potential therapy for diabetes insipidus.American journal of physiology. Renal physiology · 2018
    Review
  8. Article
  9. Review
  10. The prorenin receptor in the cardiovascular system and beyond.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  11. (Pro)Renin receptor regulates potassium homeostasis through a local mechanism.American journal of physiology. Renal physiology · 2017
    Article
  12. How Is the Brain Renin-Angiotensin System Regulated?Hypertension (Dallas, Tex. : 1979) · 2017
    Review
  13. Bradykinin/BPhysiological reports · 2017
    Article
  14. Physiology and Pathophysiology of the Intrarenal Renin-Angiotensin System: An Update.Journal of the American Society of Nephrology : JASN · 2017
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  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

2 authors at 1 institution in 1 country.

Jiqian HuangDivision of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, VA 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 expressed in renal vasculature, glomeruli, and tubules. The physiological regulation of this receptor is not well established. We hypothesized that sodium depletion increases PRR expression through cGMP- protein kinase G (PKG) signaling pathway. Renal PRR expressions were evaluated in Sprague-Dawley rats on normal sodium or low-sodium diet (LS) and in cultured rat proximal tubular cells and mouse renal inner medullary collecting duct cells exposed to LS concentration. LS augmented PRR expression in renal glomeruli, proximal tubules, distal tubules, and collecting ducts. LS also increased cGMP production and PKG activity. In cells exposed to normal sodium, cGMP analog increased PKG activity and upregulated PRR expression. In cells exposed to LS, blockade of guanylyl cyclase with 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one decreased PKG activity and downregulated PRR expression. PKG inhibition decreased phosphatase protein phosphatase 2A activity; suppressed LS-mediated phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, c-Jun, and nuclear factor-κB p65; and attenuated LS-mediated PRR upregulation. LS also enhanced DNA binding of cAMP response element binding protein 1 to cAMP response elements, nuclear factor-κB p65 to nuclear factor-κB elements, and c-Jun to activator protein 1 elements in PRR promoter in proximal tubular cells. We conclude that sodium depletion upregulates renal PRR expression via the cGMP-PKG signaling pathway by enhancing binding of cAMP response element binding protein 1, nuclear factor-κB p65, and c-Jun to PRR promotor.

Indexed as

Diet, Sodium-RestrictedAnimalsCell LineCells, CulturedCyclic AMP Response Element-Binding ProteinCyclic GMP-Dependent Protein KinasesKidneyKidney GlomerulusKidney MedullaKidney Tubules, ProximalMiceModels, AnimalNF-kappa BProrenin ReceptorProtein BindingProto-Oncogene Proteins c-junCyclic AMP Response Element-Binding ProteinCyclic GMP-Dependent Protein KinasesNF-kappa BProrenin ReceptorProto-Oncogene Proteins c-junReceptors, Cell SurfaceSodium

Identifiers

PMID22203739
PMCPMC3266459
OpenAlexW2151402328

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.