Evidence map›Paper›PMID 34207859›Full record

ReviewCells2021

Skeletal Muscle Metabolism: Origin or Prognostic Factor for Amyotrophic Lateral Sclerosis (ALS) Development?

Cyril Quessada, Alexandra Bouscary, Frédérique René, Cristiana Valle, Alberto Ferri, Shyuan T Ngo, Jean-Philippe Loeffler

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  14. Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024
    Article
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  16. Research progress on the effects of adverse exposure during pregnancy on skeletal muscle function in the offspring.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Review
  17. Review
  18. Article
  19. Review
  20. The Cellular and Molecular Signature of ALS in Muscle.Journal of personalized medicine · 2022
    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

7 authors at 3 institutions in 3 countries.

Cyril QuessadaMécanismes Centraux et Périphériques de la Neurodégénérescence, INSERM, UMR_S 1118, Centre de Recherche de Biomédecine de Strasbourg (CRBS), Université de Strasbourg, F-67000 Strasbourg, France.
Alexandra BouscaryMécanismes Centraux et Périphériques de la Neurodégénérescence, INSERM, UMR_S 1118, Centre de Recherche de Biomédecine de Strasbourg (CRBS), Université de Strasbourg, F-67000 Strasbourg, France.
Frédérique RenéMécanismes Centraux et Périphériques de la Neurodégénérescence, INSERM, UMR_S 1118, Centre de Recherche de Biomédecine de Strasbourg (CRBS), Université de Strasbourg, F-67000 Strasbourg, France.
Cristiana ValleIRCCS Fondazione Santa Lucia, Institute of Translational Pharmacology, CNR, 00133 Roma, Italy.ORCID 0000-0002-0914-6511
Alberto FerriIRCCS Fondazione Santa Lucia, Institute of Translational Pharmacology, CNR, 00133 Roma, Italy.
Shyuan T NgoAustralian Institute for Bioengineering and Nanotechnology, The University of Queensland, Brisbane, QLD 4072, Australia.
Jean-Philippe LoefflerMécanismes Centraux et Périphériques de la Neurodégénérescence, INSERM, UMR_S 1118, Centre de Recherche de Biomédecine de Strasbourg (CRBS), Université de Strasbourg, F-67000 Strasbourg, France.
Inserm · FRIstituto di Farmacologia Traslazionale · ITThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive and selective loss of motor neurons, amyotrophy and skeletal muscle paralysis usually leading to death due to respiratory failure. While generally considered an intrinsic motor neuron disease, data obtained in recent years, including our own, suggest that motor neuron protection is not sufficient to counter the disease. The dismantling of the neuromuscular junction is closely linked to chronic energy deficit found throughout the body. Metabolic (hypermetabolism and dyslipidemia) and mitochondrial alterations described in patients and murine models of ALS are associated with the development and progression of disease pathology and they appear long before motor neurons die. It is clear that these metabolic changes participate in the pathology of the disease. In this review, we summarize these changes seen throughout the course of the disease, and the subsequent impact of glucose-fatty acid oxidation imbalance on disease progression. We also highlight studies that show that correcting this loss of metabolic flexibility should now be considered a major goal for the treatment of ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsHumansMaleMuscle, SkeletalSuperoxide Dismutase-1SOD1 protein, humanSuperoxide Dismutase-1ALShypermetabolismmetabolic imbalanceneuromuscular junctionPDK4skeletal muscletrimetazidine

Identifiers

PMID34207859
PMCPMC8226541
OpenAlexW3167079526

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.