Evidence map›Paper›PMID 34064895›Full record

ReviewInternational journal of molecular sciences2021

The Role of GSK-3β in the Regulation of Protein Turnover, Myosin Phenotype, and Oxidative Capacity in Skeletal Muscle under Disuse Conditions.

Timur M Mirzoev, Kristina A Sharlo, Boris S Shenkman

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  4. Role of Peptides in Skeletal Muscle Wasting: A Scoping Review.Journal of cachexia, sarcopenia and muscle · 2025
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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

3 authors at 1 institution in 1 country.

Timur M MirzoevMyology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.ORCID 0000-0002-1986-6221
Kristina A SharloMyology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.ORCID 0000-0002-5413-6312
Boris S ShenkmanMyology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.
Institute of Biomedical Problems · RU

Funding

Program of Basic Research of the Institute of Biomedical Problems RAS 65.3Russian Science Foundation 17-75-20152
6 · The paper itself

Abstract

Skeletal muscles, being one of the most abundant tissues in the body, are involved in many vital processes, such as locomotion, posture maintenance, respiration, glucose homeostasis, etc. Hence, the maintenance of skeletal muscle mass is crucial for overall health, prevention of various diseases, and contributes to an individual's quality of life. Prolonged muscle inactivity/disuse (due to limb immobilization, mechanical ventilation, bedrest, spaceflight) represents one of the typical causes, leading to the loss of muscle mass and function. This disuse-induced muscle loss primarily results from repressed protein synthesis and increased proteolysis. Further, prolonged disuse results in slow-to-fast fiber-type transition, mitochondrial dysfunction and reduced oxidative capacity. Glycogen synthase kinase 3β (GSK-3β) is a key enzyme standing at the crossroads of various signaling pathways regulating a wide range of cellular processes. This review discusses various important roles of GSK-3β in the regulation of protein turnover, myosin phenotype, and oxidative capacity in skeletal muscles under disuse/unloading conditions and subsequent recovery. According to its vital functions, GSK-3β may represent a perspective therapeutic target in the treatment of muscle wasting induced by chronic disuse, aging, and a number of diseases.

Indexed as

Hindlimb SuspensionOxidative StressProteolysisAnimalsGlycogen Synthase Kinase 3 betaHumansMuscle, SkeletalMuscular AtrophyMyosinsPhenotypeGlycogen Synthase Kinase 3 betaMyosinsdisuseGSK-3betamuscle recoverymyosin phenotypeoxidative capacityprotein breakdownprotein synthesisskeletal muscleunloading

Identifiers

PMID34064895
PMCPMC8151958
OpenAlexW3163361654

What Socratic 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 Socratic graph.