Evidence map›Paper›PMID 26771338›Full record

ArticleJournal of hypertension2016

(Pro)renin receptor contributes to regulation of renal epithelial sodium channel.

Syed Quadri, Helmy M Siragy

Abstract read
In one paragraph

Article in Journal of hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 36 citations in OpenAlex.

  1. Plants (Basel, Switzerland) · 2026
    Article
  2. Review
  3. Article
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  5. Review
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  7. Article
  8. Soluble (Pro)Renin Receptor as a Negative Regulator of NCC (NaHypertension (Dallas, Tex. : 1979) · 2021
    Article
  9. Review
  10. Article
  11. (Pro)renin receptor in the kidney: function and significance.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019
    Review
  18. Review
  19. 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.

Syed QuadriDivision of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, Virginia, 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 DK078757NIDDK NIH HHS R01 DK078757
6 · The paper itself

Abstract

backgroundRecent studies reported increased (Pro)renin receptor (PRR) expression during low-salt intake. We hypothesized that PRR plays a role in regulation of renal epithelial sodium channel (ENaC) through serum and glucocorticoid-inducible kinase isoform 1 (SGK-1)-neural precursor cell expressed, developmentally downregulated 4-2 (Nedd4-2) signaling pathway.

methodMale Sprague-Dawley rats on normal-sodium diet and mouse renal inner medullary collecting duct cells treated with NaCl at 130  mmol/l (normal salt), or 63  mmol/l (low salt) were studied. PRR and α-ENaC expressions were evaluated 1 week after right uninephrectomy and left renal interstitial administration of 5% dextrose, scramble shRNA, or PRR shRNA (n = 6 each treatment).

resultsIn-vivo PRR shRNA significantly reduced expressions of PRR throughout the kidney and α-ENaC subunits in the renal medulla. In inner medullary collecting duct cells, low salt or angiotensin II (Ang II) augmented the mRNA and protein expressions of PRR (P < 0.05), SGK-1 (P < 0.05), and α-ENaC (P < 0.05). Low salt or Ang II increased the phosphorylation of Nedd4-2. In cells treated with low salt or Ang II, PRR siRNA significantly downregulated the mRNA and protein expressions of PRR (P < 0.05), SGK-1 (P < 0.05), and α-ENaC expression (P < 0.05).

conclusionWe conclude that PRR contributes to the regulation of α-ENaC via SGK-1-Nedd4-2 signaling pathway.

Indexed as

Angiotensin IIAnimalsCells, CulturedEndosomal Sorting Complexes Required for TransportEpithelial CellsEpithelial Sodium ChannelsGene Expression RegulationImmediate-Early ProteinsKidneyKidney Tubules, CollectingMaleMiceNedd4 Ubiquitin Protein LigasesPhosphorylationProrenin ReceptorProtein Serine-Threonine KinasesAngiotensin IIEndosomal Sorting Complexes Required for TransportEpithelial Sodium ChannelsImmediate-Early ProteinsNedd4l protein, mouseNEDD4L protein, ratNedd4 protein, ratNedd4 Ubiquitin Protein LigasesProrenin ReceptorProtein Serine-Threonine KinasesReceptors, Cell SurfaceReninRNA, MessengerSerum-Glucocorticoid Regulated KinasesSodium ChlorideUbiquitin-Protein LigasesVasoconstrictor Agents

Identifiers

PMID26771338
PMCPMC4764029
OpenAlexW2414660988

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.