Evidence map›Paper›PMID 29107290›Full record

ArticleMolecular metabolism2017

An unbiased silencing screen in muscle cells identifies miR-320a, miR-150, miR-196b, and miR-34c as regulators of skeletal muscle mitochondrial metabolism.

Dennis Dahlmans, Alexandre Houzelle, Pénélope Andreux, Johanna A Jörgensen, Xu Wang, Leon J de Windt, Patrick Schrauwen, Johan Auwerx, Joris Hoeks

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  17. Micromanaging Glucose Tolerance and Diabetes.Advanced pharmaceutical bulletin · 2017
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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

9 authors at 2 institutions in 2 countries.

Dennis DahlmansDepartment of Human Biology and Human Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, 6200MD, The Netherlands.
Alexandre HouzelleDepartment of Human Biology and Human Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, 6200MD, The Netherlands.
Pénélope AndreuxLaboratory of Integrative Systems Physiology, École polytechnique fédérale de Lausanne, Lausanne, CH-1015, Switzerland.
Johanna A JörgensenDepartment of Human Biology and Human Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, 6200MD, The Netherlands.
Xu WangLaboratory of Integrative Systems Physiology, École polytechnique fédérale de Lausanne, Lausanne, CH-1015, Switzerland.
Leon J de WindtDepartment of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, 6200MD, The Netherlands.
Patrick SchrauwenDepartment of Human Biology and Human Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, 6200MD, The Netherlands.
Johan AuwerxLaboratory of Integrative Systems Physiology, École polytechnique fédérale de Lausanne, Lausanne, CH-1015, Switzerland.
Joris HoeksDepartment of Human Biology and Human Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, 6200MD, The Netherlands. Electronic address: j.hoeks@maastrichtuniversity.nl.
Maastricht University · NLÉcole Polytechnique Fédérale de Lausanne · CH

Funding

Translational Systems Genetics of Mitochondria, Metabolism, and AgingR01AG043930 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WILLIAMS, ROBERT W. · 2013 to 2017
$2.5M
NIA NIH HHS R01 AG043930
6 · The paper itself

Abstract

objectiveStrategies improving skeletal muscle mitochondrial capacity are commonly paralleled by improvements in (metabolic) health. We and others previously identified microRNAs regulating mitochondrial oxidative capacity, but data in skeletal muscle are limited. Therefore, the present study aimed to identify novel microRNAs regulating skeletal muscle mitochondrial metabolism. METHODS AND

resultsWe conducted an unbiased, hypothesis-free microRNA silencing screen in C2C12 myoblasts, using >700 specific microRNA inhibitors, and investigated a broad panel of mitochondrial markers. After subsequent validation in differentiated C2C12 myotubes, and exclusion of microRNAs without a human homologue or with an adverse effect on mitochondrial metabolism, 19 candidate microRNAs remained. Human clinical relevance of these microRNAs was investigated by measuring their expression in human skeletal muscle of subject groups displaying large variation in skeletal muscle mitochondrial capacity.

conclusionThe results show that that microRNA-320a, microRNA-196b-3p, microRNA-150-5p, and microRNA-34c-3p are tightly related to in vivo skeletal muscle mitochondrial function in humans and identify these microRNAs as targets for improving mitochondrial metabolism.

Indexed as

AnimalsCell DifferentiationCell LineHumansMaleMiceMicroRNAsMitochondria, MuscleMuscle Fibers, SkeletalMuscle, SkeletalMyoblasts, Smooth MuscleMicroRNAsMicroRNAMitochondriaOxidative capacityScreeningSkeletal muscle metabolismType 2 diabetes

Identifiers

PMID29107290
PMCPMC5681243
OpenAlexW2750862143

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.