Special Issue "Molecular Biology of Skeletal Muscle Regeneration and Adaptation"

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 1378

Special Issue Editor

Department of Biochemistry, University of Szeged, Szeged, Hungary
Interests: biochemistry and molecular biology of skeletal muscle regeneration and adaptation

Special Issue Information

Dear Colleagues,

Skeletal muscle is the largest tissue in mammals, contributing  about 40% of their total body mass. This entity shows remarkable variation and is exposed to numerous environmental constraints and pathological conditions. How does the skeletal muscle face these challenges? What algorithms maintain integrity after trial runs or detrimental conditions? The answers have been sought for several decades, first in vitro and, later, in combined studies. As a result, skeletal muscle became a favorite object of differentiation molecular biology. It has inseminated the field of heart muscle adaptation and helped to form a more realistic view of heart regeneration. Skeletal muscle regeneration is well suited for differential gene expression studies. First the transcription factors and later the signal pathways were sought out with remarkable success; the revealed complexity explained a lot about phenotypical variations. The pivotal roles of non-muscle components such as extracellular tissue and inflammatory and angiogenic cells have been found in addition to the nerves’ influence.

In this planned Special Issue, we welcome any submissions on the topic of molecular biology of skeletal muscle regeneration and adaptation. Since this topic belongs to the field of differentiation, studies that investigate morphology and phenotype with molecular changes are especially welcome. Approaches focusing primarily on the molecular biology of non-muscle cells in skeletal muscle regeneration and adaptation are also encouraged. Both reviews and original contributions will be considered.

Prof. Dr. Ernő Zádor 
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2300 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • skeletal muscle
  • regeneration
  • adaptation

Published Papers (1 paper)

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Review

Review
Alcohol, Resistance Exercise, and mTOR Pathway Signaling: An Evidence-Based Narrative Review
Biomolecules 2023, 13(1), 2; https://doi.org/10.3390/biom13010002 - 20 Dec 2022
Viewed by 1138
Abstract
Skeletal muscle mass is determined by the balance between muscle protein synthesis (MPS) and degradation. Several intracellular signaling pathways control this balance, including mammalian/mechanistic target of rapamycin (mTOR) complex 1 (C1). Activation of this pathway in skeletal muscle is controlled, in part, by [...] Read more.
Skeletal muscle mass is determined by the balance between muscle protein synthesis (MPS) and degradation. Several intracellular signaling pathways control this balance, including mammalian/mechanistic target of rapamycin (mTOR) complex 1 (C1). Activation of this pathway in skeletal muscle is controlled, in part, by nutrition (e.g., amino acids and alcohol) and exercise (e.g., resistance exercise (RE)). Acute and chronic alcohol use can result in myopathy, and evidence points to altered mTORC1 signaling as a contributing factor. Moreover, individuals who regularly perform RE or vigorous aerobic exercise are more likely to use alcohol frequently and in larger quantities. Therefore, alcohol may antagonize beneficial exercise-induced increases in mTORC1 pathway signaling. The purpose of this review is to synthesize up-to-date evidence regarding mTORC1 pathway signaling and the independent and combined effects of acute alcohol and RE on activation of the mTORC1 pathway. Overall, acute alcohol impairs and RE activates mTORC1 pathway signaling; however, effects vary by model, sex, feeding, training status, quantity, etc., such that anabolic stimuli may partially rescue the alcohol-mediated pathway inhibition. Likewise, the impact of alcohol on RE-induced mTORC1 pathway signaling appears dependent on several factors including nutrition and sex, although many questions remain unanswered. Accordingly, we identify gaps in the literature that remain to be elucidated to fully understand the independent and combined impacts of alcohol and RE on mTORC1 pathway signaling. Full article
(This article belongs to the Special Issue Molecular Biology of Skeletal Muscle Regeneration and Adaptation)
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