Evidence map›Paper›PMID 30126255›Full record

ArticleInternational journal of molecular sciences2018

Upregulation of Nrf2 and Decreased Redox Signaling Contribute to Renoprotective Effects of Chemerin Receptor Blockade in Diabetic Mice.

Karla Bianca Neves, Augusto Cesar Montezano, Rheure Alves-Lopes, Thiago Bruder-Nascimento, Rafael Menezes Costa, Roberto S Costa, Rhian M Touyz, Rita C Tostes

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Vascular Stress Signaling in Hypertension.Circulation research · 2021
    Review
  8. Article
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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 2 institutions in 2 countries.

Karla Bianca NevesDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil. Karla.Neves@glasgow.ac.uk.ORCID 0000-0001-5158-9263
Augusto Cesar MontezanoInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8TA, UK. Augusto.Montezano@glasgow.ac.uk.
Rheure Alves-LopesDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil. Rheure.Lopes@glasgow.ac.uk.
Thiago Bruder-NascimentoDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil. bruderthiago@yahoo.com.br.
Rafael Menezes CostaDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil. rafael.menezess@yahoo.com.br.
Roberto S CostaDepartment of Pathology and Legal Medicine, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14040-900, Brazil. rscosta@fmrp.usp.br.
Rhian M TouyzInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8TA, UK. Rhian.Touyz@glasgow.ac.uk.
Rita C TostesDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil. rtostes@usp.com.
Universidade de São Paulo · BRUniversity of Glasgow · GB

Funding

British Heart Foundation CH/12/4/29762
6 · The paper itself

Abstract

Chemerin, acting through its receptor ChemR23, is an adipokine associated with inflammatory response, glucose and lipid metabolism and vascular function. Although this adipokine has been associated with the development and progression of kidney disease, it is not clear whether the chemerin/ChemR23 system plays a role in renal function in the context of diabetes. Therefore, we sought to determine whether ChemR23 receptor blockade prevents the development and/or progression of diabetic nephropathy and questioned the role of oxidative stress and Nrf2 in this process. Renal redox state and function were assessed in non-diabetic lean db/m and diabetic obese db/db mice treated with vehicle or CCX832 (ChemR23 antagonist). Renal reactive oxygen species (ROS) production, which was increased in diabetic mice, was attenuated by CCX832. This was associated with an increase in Nox 4 expression. Augmented protein oxidation in db/db mice was not observed when mice were treated with CCX832.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesKidneyMaleMiceMice, Inbred C57BLNF-E2-Related Factor 2Oxidation-ReductionOxidative StressReceptors, G-Protein-CoupledGPR1 protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2Receptors, G-Protein-CoupledchemerinChemR23kidneyoxidative stresstype 2 diabetes

Identifiers

PMID30126255
PMCPMC6121242
OpenAlexW2886654052

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.