Evidence map›Paper›PMID 31025018›Full record

ArticleHeliyon2019

Effect of (-)-epicatechin on the modulation of progression markers of chronic renal damage in a 5/6 nephrectomy experimental model.

Jorge Montes-Rivera, Mónica Arellano-Mendoza, Nayelli Nájera, Leonardo Del Valle-Mondragón, Francisco Villarreal, Ivan Rubio-Gayosso, Javier Perez-Duran, Eduardo Meaney, Guillermo Ceballos

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

9 authors at 3 institutions in 2 countries.

Jorge Montes-RiveraLaboratorio de Investigación Integral Cardiometabólica, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Mónica Arellano-MendozaLaboratorio de Investigación en Enfermedades Crónico Degenerativas, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Nayelli NájeraLaboratorio de Investigación Integral Cardiometabólica, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Leonardo Del Valle-MondragónDepartamento de Farmacología, Instituto Nacional de Cardiología "Ignacio Chávez", Ciudad de México, Mexico.
Francisco VillarrealUniversity of California at San Diego, USA.
Ivan Rubio-GayossoLaboratorio de Investigación Integral Cardiometabólica, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Javier Perez-DuranLaboratorio de Investigación Integral Cardiometabólica, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Eduardo MeaneyLaboratorio de Investigación Integral Cardiometabólica, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Guillermo CeballosLaboratorio de Investigación Integral Cardiometabólica, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México, 11340, Mexico.
Instituto Politécnico Nacional · MXInstituto Nacional de Cardiología · MXUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo evaluate the effects of (-)-epicatechin (Epi) in the progression of kidney damage. MATERIAL AND

methodsWe assessed the effects of Epi [0.01-20 mg/kg of body weight/day] during 14 days, in a 5/6 nephrectomy model in mice. KEY

findingsNephrectomy-induced systolic arterial hypertension was significantly reduced in a dose dependent manner with Epi treatment. Increased serum creatinine and urea were reduced almost to normal values. The concentration of tetrahydrobiopterin (BH4), used as subrogate of endothelial dysfunction, decreased in nephrectomyzed animals, Epi treatment increased BH4 levels almost reaching normal values. The expression of angiotensin II receptor (AT SIGNIFICANCE: Chronic kidney disease (CKD) is an independent cardiovascular risk factor associated with a mortality rate 10 to 20 times higher than that of the general population. High blood pressure, endothelial dysfunction and oxidative stress are important factors determining kidney damage progression. Findings of this study indicate that Epi is able to counteract the deleterious effects of subtotal nephrectomy and the structural and functional changes in the remnant kidney tissue, decreasing the progression of CKD. These results warrant the possibility of implement clinical trials to limit the progression of CKD in humans.

Indexed as

Cell biologyPathology

Identifiers

PMID31025018
PMCPMC6475891
OpenAlexW2940343210

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.