Evidence map›Paper›PMID 32371010›Full record

ReviewRedox biology2020

Redox modulation of muscle mass and function.

M C Gomez-Cabrera, C Arc-Chagnaud, A Salvador-Pascual, T Brioche, A Chopard, G Olaso-Gonzalez, J Viña

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-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

33 citing papers in PubMed, 53 citations in OpenAlex.

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  17. 5'-Cytimidine Monophosphate Ameliorates HAntioxidants (Basel, Switzerland) · 2024
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  19. The adaptive antioxidant response during fasting-induced muscle atrophy is oppositely regulated by ZEB1 and ZEB2.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

7 authors at 3 institutions in 3 countries.

M C Gomez-CabreraFreshage Research Group, Department of Physiology. Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain.
C Arc-ChagnaudFreshage Research Group, Department of Physiology. Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain; INRA, UMR866 Dynamique Musculaire et Métabolisme, Université de Montpellier, F-34060, Montpellier, France.
A Salvador-PascualFreshage Research Group, Department of Physiology. Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain; Department of Integrative Biology, University of California, Berkeley, CA, 94705, USA.
T BriocheINRA, UMR866 Dynamique Musculaire et Métabolisme, Université de Montpellier, F-34060, Montpellier, France.
A ChopardINRA, UMR866 Dynamique Musculaire et Métabolisme, Université de Montpellier, F-34060, Montpellier, France.
G Olaso-GonzalezFreshage Research Group, Department of Physiology. Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain. Electronic address: gloria.olaso@uv.es.
J ViñaFreshage Research Group, Department of Physiology. Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain.
Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable · ESUniversitat de València · ESUniversité de Montpellier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle mass and strength are very important for exercise performance. Training-induced musculoskeletal injuries usually require periods of complete immobilization to prevent any muscle contraction of the affected muscle groups. Disuse muscle wasting will likely affect every sport practitioner in his or her lifetime. Even short periods of disuse results in significant declines in muscle size, fiber cross sectional area, and strength. To understand the molecular signaling pathways involved in disuse muscle atrophy is of the utmost importance to develop more effective countermeasures in sport science research. We have divided our review in four different sections. In the first one we discuss the molecular mechanisms involved in muscle atrophy including the main protein synthesis and protein breakdown signaling pathways. In the second section of the review we deal with the main cellular, animal, and human atrophy models. The sources of reactive oxygen species in disuse muscle atrophy and the mechanism through which they regulate protein synthesis and proteolysis are reviewed in the third section of this review. The last section is devoted to the potential interventions to prevent muscle disuse atrophy with especial consideration to studies on which the levels of endogenous antioxidants enzymes or dietary antioxidants have been tested.

Indexed as

Muscle, SkeletalMuscular AtrophyAnimalsAntioxidantsHumansOxidation-ReductionReactive Oxygen SpeciesAntioxidantsReactive Oxygen Species

Identifiers

PMID32371010
PMCPMC7284907
OpenAlexW3017352469

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.