Evidence map›Paper›PMID 33893273›Full record

ArticleNature communications2021

VPS39-deficiency observed in type 2 diabetes impairs muscle stem cell differentiation via altered autophagy and epigenetics.

Cajsa Davegårdh, Johanna Säll, Anna Benrick, Christa Broholm, Petr Volkov, Alexander Perfilyev, Tora Ida Henriksen, Yanling Wu, Line Hjort, Charlotte Brøns and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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  13. Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 11 institutions in 5 countries.

Cajsa Davegårdh *Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden.ORCID http://orcid.org/0000-0003-1124-7570
Johanna Säll *Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden.ORCID http://orcid.org/0000-0001-7337-4140
Anna Benrick *Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Christa BroholmDiabetes and Bone-metabolic Research Unit, Department of Endocrinology, Rigshospitalet, Copenhagen, Denmark.
Petr VolkovEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden.
Alexander PerfilyevEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden.ORCID http://orcid.org/0000-0003-1136-8946
Tora Ida HenriksenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Yanling WuDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Line HjortDiabetes and Bone-metabolic Research Unit, Department of Endocrinology, Rigshospitalet, Copenhagen, Denmark.
Charlotte BrønsDiabetes and Bone-metabolic Research Unit, Department of Endocrinology, Rigshospitalet, Copenhagen, Denmark.
Ola HanssonGenomics, Diabetes and Endocrinology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.ORCID http://orcid.org/0000-0002-7394-7639
Maria PedersenThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Jens U WürthnerADC Therapeutics, Biopole, Epalinges, Switzerland.
Klaus PfefferInstitute of Medical Microbiology and Hospital Hygiene, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Emma NilssonEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden.
Allan VaagSteno Diabetes Center Copenhagen, Gentofte, Denmark.
Elisabet Stener-VictorinDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-3424-1502
Karolina PircsLaboratory of Molecular Neurogenetics, Department of Experimental Medical Science, Wallenberg Neuroscience Center and Lund Stem Cell Center, Lund University, Lund, Sweden.
Camilla ScheeleThe Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Charlotte LingEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden. charlotte.ling@med.lu.se.ORCID http://orcid.org/0000-0003-0587-7154
Scania (Sweden) · SERigshospitalet · DKUniversity of Copenhagen · DKAdc Therapeutics (Switzerland) · CHHeinrich Heine University Düsseldorf · DEKarolinska Institutet · SELund University · SESteno Diabetes Centers · DKUniversity of Gothenburg · SEUniversity of Helsinki · FIUniversity of Skövde · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance and lower muscle quality (strength divided by mass) are hallmarks of type 2 diabetes (T2D). Here, we explore whether alterations in muscle stem cells (myoblasts) from individuals with T2D contribute to these phenotypes. We identify VPS39 as an important regulator of myoblast differentiation and muscle glucose uptake, and VPS39 is downregulated in myoblasts and myotubes from individuals with T2D. We discover a pathway connecting VPS39-deficiency in human myoblasts to impaired autophagy, abnormal epigenetic reprogramming, dysregulation of myogenic regulators, and perturbed differentiation. VPS39 knockdown in human myoblasts has profound effects on autophagic flux, insulin signaling, epigenetic enzymes, DNA methylation and expression of myogenic regulators, and gene sets related to the cell cycle, muscle structure and apoptosis. These data mimic what is observed in myoblasts from individuals with T2D. Furthermore, the muscle of Vps39

Indexed as

AnimalsAutophagyAutophagy-Related ProteinsCell DifferentiationCells, CulturedDiabetes Mellitus, Type 2Epigenesis, GeneticEpigenomicsFemaleGene Expression ProfilingHumansMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedAutophagy-Related ProteinsVesicular Transport ProteinsVPS39 protein, human

Identifiers

PMID33893273
PMCPMC8065135
OpenAlexW3154175795

What Socratic holds

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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 Socratic graph.