Evidence map›Paper›PMID 25101263›Full record

ArticleBioMed research international2014

Effect of angiotensin II and small GTPase Ras signaling pathway inhibition on early renal changes in a murine model of obstructive nephropathy.

Ana B Rodríguez-Peña, Isabel Fuentes-Calvo, Neil G Docherty, Miguel Arévalo, María T Grande, Nélida Eleno, Fernando Pérez-Barriocanal, José M López-Novoa

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. The molecular biology of pelvi-ureteric junction obstruction.Pediatric nephrology (Berlin, Germany) · 2018
    Review
  6. Article
  7. Review
  8. 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

8 authors at 5 institutions in 2 countries.

Ana B Rodríguez-PeñaUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain ; Centro de Investigación del Cáncer (CSIC), Universidad de Salamanca, 37007 Salamanca, Spain.
Isabel Fuentes-CalvoUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain.
Neil G DochertyUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain ; Diabetes Complications Research Centre, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Miguel ArévaloInstituto de Investigaciones Biomédicas de Salamanca (IBSAL), 37007 Salamanca, Spain ; Departamento de Anatomía e Histología Humanas, Universidad de Salamanca, 37007 Salamanca, Spain.
María T GrandeUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain ; Universidad Francisco de Vitoria, 28223 Madrid, Spain.
Nélida ElenoUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain ; Instituto de Investigaciones Biomédicas de Salamanca (IBSAL), 37007 Salamanca, Spain.
Fernando Pérez-BarriocanalUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain ; Instituto de Investigaciones Biomédicas de Salamanca (IBSAL), 37007 Salamanca, Spain.
José M López-NovoaUnidad de Fisiopatología Renal y Cardiovascular, Instituto "Reina Sofía" de Investigación Nefrológica, Fundación Renal Iñigo Alvarez de Toledo, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain ; Instituto de Investigaciones Biomédicas de Salamanca (IBSAL), 37007 Salamanca, Spain.
Universidad de Salamanca · ESInstituto de Investigación Biomédica de Salamanca · ESCentro de Investigación del Cáncer · ESFundación Renal · ESUniversidad Francisco de Vitoria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulointerstitial fibrosis is a major feature of chronic kidney disease. Unilateral ureteral obstruction (UUO) in rodents leads to the development of renal tubulointerstitial fibrosis consistent with histopathological changes observed in advanced chronic kidney disease in humans. The purpose of this study was to assess the effect of inhibiting angiotensin II receptors or Ras activation on early renal fibrotic changes induced by UUO. Animals either received angiotensin II or underwent UUO. UUO animals received either losartan, atorvastatin, and farnesyl transferase inhibitor (FTI) L-744,832, or chaetomellic acid A (ChA). Levels of activated Ras, phospho-ERK1/2, phospho-Akt, fibronectin, and α-smooth muscle actin were subsequently quantified in renal tissue by ELISA, Western blot, and/or immunohistochemistry. Our results demonstrate that administration of angiotensin II induces activation of the small GTPase Ras/Erk/Akt signaling system, suggesting an involvement of angiotensin II in the early obstruction-induced activation of renal Ras. Furthermore, upstream inhibition of Ras signalling by blocking either angiotensin AT1 type receptor or by inhibiting Ras prenylation (atorvastatin, FTI o ChA) reduced the activation of the Ras/Erk/Akt signaling system and decreased the early fibrotic response in the obstructed kidney. This study points out that pharmacological inhibition of Ras activation may hold promise as a future strategy in the prevention of renal fibrosis.

Indexed as

Angiotensin IIAnimalsAtorvastatinDisease Models, AnimalFibrosisHeptanoic AcidsHumansKidneyKidney DiseasesMiceMonomeric GTP-Binding ProteinsPyrrolesReceptor, Angiotensin, Type 1Signal TransductionUreteral ObstructionAngiotensin IIAtorvastatinHeptanoic AcidsMonomeric GTP-Binding ProteinsPyrrolesReceptor, Angiotensin, Type 1

Identifiers

PMID25101263
PMCPMC4101960
OpenAlexW2162858008

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.