Evidence map›Paper›PMID 31690958›Full record

ArticleUrolithiasis2020

Nox1-derived oxidative stress as a common pathogenic link between obesity and hyperoxaluria-related kidney injury.

J Sáenz-Medina, M Muñoz, A Sanchez, C Rodriguez, E Jorge, C Corbacho, D Izquierdo, M Santos, E Donoso, E Virumbrales and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Urolithiasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Cross-Talk of NADPH Oxidases and Inflammation in Obesity.Antioxidants (Basel, Switzerland) · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. 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

15 authors at 3 institutions in 1 country.

J Sáenz-MedinaDepartment of Urology, Hospital Universitario Puerta de Hierro-Majadahonda, Universidad Rey Juan Carlos, Calle Manuel de Falla, 1, Majadahonda, 28222, Madrid, Spain. javiersaenzmedina@yahoo.es.ORCID http://orcid.org/0000-0002-8568-854X
M MuñozDepartment of Physiology, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.
A SanchezDepartment of Physiology, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.
C RodriguezDepartment of Physiology, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.
E JorgeDepartment of Clinical Biochemistry, Hospital Universitario Puerta de Hierro-Majadahonda, Madrid, Spain.
C CorbachoDepartment of Pathology, Hospital Universitario Puerta de Hierro-Majadahonda, Madrid, Spain.
D IzquierdoDepartment of Pathology, Hospital Universitario Puerta de Hierro-Majadahonda, Madrid, Spain.
M SantosMedical and Surgical Research Facility, Instituto de Investigación Sanitaria Puerta de Hierro, Madrid, Spain.
E DonosoDepartment of Clinical Biochemistry, Hospital Universitario Puerta de Hierro-Majadahonda, Madrid, Spain.
E VirumbralesDepartment of Clinical Biochemistry, Hospital Universitario Puerta de Hierro-Majadahonda, Madrid, Spain.
A SanchezBiobank, Instituto de Investigación Sanitaria Puerta de Hierro, Madrid, Spain.
E RamilMolecular Biology and DNA Sequencing Facility, Instituto de Investigación Sanitaria Puerta de Hierro, Madrid, Spain.
M J CoronadoConfocal Microscopy Facility, Instituto de Investigación Sanitaria Puerta de Hierro, Madrid, Spain.
D PrietoDepartment of Physiology, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.
J CarballidoDepartment of Urology, Hospital Universitario Puerta de Hierro-Majadahonda, Universidad Autónoma de Madrid, Madrid, Spain.
Hospital Universitario Puerta de Hierro Majadahonda · ESUniversidad Complutense de Madrid · ESUniversidad Rey Juan Carlos · ES

Funding

Ministerio de Economía y Competitividad SAF2016-77526-R
6 · The paper itself

Abstract

Specific relationships among reactive oxygen species, activation pathways, and inflammatory mechanisms involved in kidney injury were assessed in a combined model of obesity and hyperoxaluria. Male Wistar rats were divided into four groups: Control, HFD (high fat diet), OX (0.75% ethylene glycol), and HFD + OX (combined model) Changes in basal O

Indexed as

AnimalsDisease Models, AnimalHyperoxaluriaKidney DiseasesMaleNADPH Oxidase 1ObesityOxidative StressRatsRats, WistarNADPH Oxidase 1NOX1 protein, ratNADPH oxidaseObesityOxidative stressRenal injuryUrolithiasis

Identifiers

PMID31690958
OpenAlexW2983508144

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.