Evidence map›Paper›PMID 31160616›Full record

ArticleScientific reports2019

Dysregulated autophagy in muscle precursor cells from humans with type 2 diabetes.

T I Henriksen, L V Wigge, J Nielsen, B K Pedersen, M Sandri, C Scheele

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Biophysics reviews · 2022
    Review
  9. Polycystin-2 (PC2) is a key determinant of in vitro myogenesis.American journal of physiology. Cell physiology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mitochondrial Function in Muscle Stem Cell Fates.Frontiers in cell and developmental biology · 2020
    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

6 authors at 3 institutions in 3 countries.

T I HenriksenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. torahenriksen@sund.ku.dk.ORCID http://orcid.org/0000-0003-1568-8920
L V WiggeDepartment of Biology and Biological Engineering, Chalmers University of Technology, 41296, Gothenburg, Sweden.
J NielsenDepartment of Biology and Biological Engineering, Chalmers University of Technology, 41296, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-9955-6003
B K PedersenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-6508-6288
M SandriVenetian Institute of Molecular Medicine, via Orus 2, 35129, Padova, Italy.
C ScheeleThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-6055-9709
University of Copenhagen · DKChalmers University of Technology · SEVeneto Institute of Molecular Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is active during cellular remodeling including muscle differentiation. Muscle differentiation is dysregulated in type 2 diabetes and we therefore hypothesize that muscle precursor cells from people with type 2 diabetes (T2DM) have a dysregulation of their autophagy leading to impaired myogenesis. Muscle precursor cells were isolated from people with T2DM or healthy controls and differentiated in vitro. Autophagy marker levels were assessed by immunoblotting. Differentially expressed autophagy-related genes between healthy and T2DM groups were identified based on a previously published RNA-sequencing data-set, which we verified by RT-qPCR. siRNA was used to assess the function of differentially expressed autophagy genes. Basal autophagy increases during human muscle differentiation, while T2DM muscle cells have reduced levels of autophagy marker ATG7 and show a blunted response to starvation. Moreover, we demonstrate that the 3 non-canonical autophagy genes DRAM1, VAMP8 and TP53INP1 as differentially expressed between healthy and T2DM groups during myoblast differentiation, and that T53INP1 knock-down alters expression of both pro-and anti-apoptotic genes. In vitro differentiated T2DM muscle cells show differential expression of autophagy-related genes. These genes do not regulate myogenic transcription factors but may rather be involved in p53-associated myoblast apoptosis during early myogenesis.

Indexed as

AgedApoptosisAutophagyAutophagy-Related Protein 7BiopsyCarrier ProteinsCell DifferentiationDiabetes Mellitus, Type 2Gene Expression RegulationGene Expression Regulation, DevelopmentalHeat-Shock ProteinsHumansMaleMembrane ProteinsMiddle AgedMuscle DevelopmentAutophagy-Related Protein 7Carrier ProteinsDRAM1 protein, humanHeat-Shock ProteinsMembrane ProteinsR-SNARE ProteinsTP53INP1 protein, humanTumor Suppressor Protein p53VAMP8 protein, human

Identifiers

PMID31160616
PMCPMC6546785
OpenAlexW2948012344

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.