Evidence map›Paper›PMID 28702332›Full record

ArticleMolecular metabolism2017

Dysregulation of a novel miR-23b/27b-p53 axis impairs muscle stem cell differentiation of humans with type 2 diabetes.

Tora I Henriksen, Peter K Davidsen, Maria Pedersen, Heidi S Schultz, Ninna S Hansen, Therese J Larsen, Allan Vaag, Bente K Pedersen, Søren Nielsen, Camilla Scheele

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 30 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

10 authors at 3 institutions in 2 countries.

Tora I HenriksenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Peter K DavidsenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Maria PedersenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Heidi S SchultzNovo Nordisk A/S, Måløv, Denmark.
Ninna S HansenDepartment of Endocrinology, Diabetes and Metabolism, Rigshospitalet, Copenhagen, Denmark.
Therese J LarsenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Allan VaagDepartment of Endocrinology, Diabetes and Metabolism, Rigshospitalet, Copenhagen, Denmark.
Bente K PedersenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Søren NielsenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Camilla ScheeleThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen Denmark.
Rigshospitalet · DKUniversity of Copenhagen · DKNovo Nordisk (Denmark) · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMicroRNAs (miRNAs) are increasingly recognized as fine-tuning regulators of metabolism, and are dysregulated in several disease conditions. With their capacity to rapidly change gene expression, miRNAs are also important regulators of development and cell differentiation. In the current study, we describe an impaired myogenic capacity of muscle stem cells isolated from humans with type 2 diabetes (T2DM) and assess whether this phenotype is regulated by miRNAs.

methodsWe measured global miRNA expression during in vitro differentiation of muscle stem cells derived from T2DM patients and healthy controls.

resultsThe mir-23b/27b cluster was downregulated in the cells of the patients, and a pro-myogenic effect of these miRNAs was mediated through the p53 pathway, which was concordantly dysregulated in the muscle cells derived from humans with T2DM.

conclusionsOur results indicate that we have identified a novel pathway for coordination of myogenesis, the miR-23b/27b-p53 axis that, when dysregulated, potentially contributes to a sustained muscular dysfunction in T2DM.

Indexed as

Cell DifferentiationAgedCells, CulturedDiabetes Mellitus, Type 2Down-RegulationFemaleHumansMaleMicroRNAsMiddle AgedMuscle DevelopmentMyoblasts, SkeletalTumor Suppressor Protein p53MicroRNAsMIRN23a microRNA, humanMIRN27 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53DiabetesHumanMicroRNAmiR-23bmiR-27bMusclemuscle stem cellsMyogenesisp53Satellite cell

Identifiers

PMID28702332
PMCPMC5485225
OpenAlexW2608802248

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.