Evidence map›Paper›PMID 28755631›Full record

ArticleRedox biology2017

Upregulation of UCP2 in beta-cells confers partial protection against both oxidative stress and glucotoxicity.

Ning Li, Melis Karaca, Pierre Maechler

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Ning LiDepartment of Cell Physiology and Metabolism & Faculty Diabetes Center, University of Geneva Medical Center, 1 rue Michel-Servet, 1206 Geneva, Switzerland.
Melis KaracaDepartment of Cell Physiology and Metabolism & Faculty Diabetes Center, University of Geneva Medical Center, 1 rue Michel-Servet, 1206 Geneva, Switzerland.
Pierre MaechlerDepartment of Cell Physiology and Metabolism & Faculty Diabetes Center, University of Geneva Medical Center, 1 rue Michel-Servet, 1206 Geneva, Switzerland. Electronic address: Pierre.Maechler@unige.ch.
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deterioration of pancreatic beta-cells plays a critical role in the development of type 2 diabetes. Among the various stressors contributing to these deleterious effects, glucotoxicity and superoxides have been proposed as major players. In this context, the mitochondrial uncoupling protein UCP2 is regularly associated with the stress response. In the present study, we tested the effects of UCP2 upregulation in mouse islets with beta-cell specific overexpression of UCP2 (RIP-UCP2). Islets were subjected to both chronic glucotoxicity (7 days at 30mM glucose) and acute oxidative stress (200µM H

Indexed as

Oxidative StressAdenosine TriphosphateAnimalsCell DeathCells, CulturedGlucoseInsulin-Secreting CellsMembrane Potential, MitochondrialMiceMice, Inbred C57BLUncoupling Protein 2Up-RegulationAdenosine TriphosphateGlucoseUcp2 protein, mouseUncoupling Protein 2Beta-cellGlucotoxicityInsulin secretionOxidative stressPancreatic isletUCP2

Identifiers

PMID28755631
PMCPMC5537434
OpenAlexW2738278588

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.