Evidence map›Paper›PMID 31320589›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

BDNF is a mediator of glycolytic fiber-type specification in mouse skeletal muscle.

Julien Delezie, Martin Weihrauch, Geraldine Maier, Rocío Tejero, Daniel J Ham, Jonathan F Gill, Bettina Karrer-Cardel, Markus A Rüegg, Lucía Tabares, Christoph Handschin

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 3 pooled it
6.3field-weighted citation impact, top 3% 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

94 citing papers in PubMed, 3 syntheses or guidelines pooled it, 137 citations in OpenAlex.

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34 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Julien DelezieBiozentrum, University of Basel, CH-4056 Basel, Switzerland.ORCID 0000-0002-1350-8423
Martin WeihrauchBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Geraldine MaierBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Rocío TejeroDepartment of Medical Physiology and Biophysics, School of Medicine, University of Seville, 41009 Seville, Spain.
Daniel J HamBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Jonathan F GillBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Bettina Karrer-CardelBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Markus A RüeggBiozentrum, University of Basel, CH-4056 Basel, Switzerland.ORCID 0000-0002-4974-9384
Lucía TabaresDepartment of Medical Physiology and Biophysics, School of Medicine, University of Seville, 41009 Seville, Spain.
Christoph HandschinBiozentrum, University of Basel, CH-4056 Basel, Switzerland; christoph.handschin@unibas.ch.ORCID 0000-0003-0603-1097
University of Basel · CHUniversidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) influences the differentiation, plasticity, and survival of central neurons and likewise, affects the development of the neuromuscular system. Besides its neuronal origin, BDNF is also a member of the myokine family. However, the role of skeletal muscle-derived BDNF in regulating neuromuscular physiology in vivo remains unclear. Using gain- and loss-of-function animal models, we show that muscle-specific ablation of BDNF shifts the proportion of muscle fibers from type IIB to IIX, concomitant with elevated slow muscle-type gene expression. Furthermore, BDNF deletion reduces motor end plate volume without affecting neuromuscular junction (NMJ) integrity. These morphological changes are associated with slow muscle function and a greater resistance to contraction-induced fatigue. Conversely, BDNF overexpression promotes a fast muscle-type gene program and elevates glycolytic fiber number. These findings indicate that BDNF is required for fiber-type specification and provide insights into its potential modulation as a therapeutic target in muscle diseases.

Indexed as

GlycolysisAnimalsBrain-Derived Neurotrophic FactorGaitGene Expression RegulationLocomotionMice, KnockoutModels, BiologicalMotor EndplateMuscle ContractionMuscle FatigueMuscle Fibers, SkeletalOrgan SpecificityOxidation-ReductionPhysical Conditioning, AnimalSignal TransductionBrain-Derived Neurotrophic Factorendurance exercisemyokineneuromuscular junctionneurotrophic factoroxidative fiber

Identifiers

PMID31320589
PMCPMC6690026
OpenAlexW2959540491

What OpenQuestion holds

Textmetadata
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.