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Molecular Mechanisms of Skeletal Muscle Metabolism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 1166

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Guest Editor
Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Florence, 50134 Firenze, Italy
Interests: antioxidants; vegetable-derived compounds; vitamins; skeletal muscle; chronic diseases; aging; signalling pathway effectors; subcellular compartments; mitochondria; cytoskeleton
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Special Issue Information

Dear Colleagues,

Skeletal muscle (SkM) is critical for the generation of mechanical force and the support of bodily posture and movement. However, in recent years, the relevance of SkM functions as a regulator of whole-body metabolism, especially carbohydrate and lipid metabolism, has been studied. Although this interest is mainly due to its contribution to resting energy expenditure, insulin-mediated glucose disposal and body mass, the role of SkM in lipid metabolism is underestimated. Interestingly, SkM metabolic capacity is correlated with the types of fibers and acute and chronic contraction. In fact, in response to exercise, leading to an increase in energy turnover, changes even greater than 100-fold can occur.

In addition, SkM acts also as an endocrine organ releasing peptides, known as exokines, that act in a paracrine manner; thus, SkM can also modulate the functions and metabolism in other organs.

In this Special Issue, high-quality original research and reviews are welcome, as they could help us to better understand the cellular mechanisms underlying glucose and lipid metabolism inside SkM and the potential crosstalk between SkM modulators and the effects of released myokines on other organs during exercise, as well as in patients with obesity and other pathological conditions. Reporting advances in SkM metabolic capacity in aging and sex differences is also encouraged.

Prof. Dr. Elisabetta Meacci
Guest Editor

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Keywords

  • skeletal muscle
  • metabolism
  • aging
  • skeletal muscle atrophy
  • bioactive lipids
  • oxidative stress
  • biomarkers

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Published Papers (1 paper)

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Research

17 pages, 3816 KiB  
Article
SMURF1-Induced Ubiquitination of FTH1 Disrupts Iron Homeostasis and Suppresses Myogenesis
by Xia Xiong, Wen Li, Chunlin Yu, Mohan Qiu, Zengrong Zhang, Chenming Hu, Shiliang Zhu, Li Yang, Han Pen, Xiaoyan Song, Jialei Chen, Bo Xia, Shunshun Han and Chaowu Yang
Int. J. Mol. Sci. 2025, 26(3), 1390; https://doi.org/10.3390/ijms26031390 - 6 Feb 2025
Cited by 1 | Viewed by 879
Abstract
Ferritin heavy chain 1 (FTH1) is pivotal in the storage, release, and utilization of iron, plays a crucial role in the ferroptosis pathway, and exerts significant impacts on various diseases. Iron influences skeletal muscle development and health by promoting cell growth, ensuring energy [...] Read more.
Ferritin heavy chain 1 (FTH1) is pivotal in the storage, release, and utilization of iron, plays a crucial role in the ferroptosis pathway, and exerts significant impacts on various diseases. Iron influences skeletal muscle development and health by promoting cell growth, ensuring energy metabolism and ATP synthesis, maintaining oxygen supply, and facilitating protein synthesis. However, the precise molecular mechanisms underlying iron’s regulation of skeletal muscle growth and development remain elusive. In this study, we demonstrated that the conditional knockout (cKO) of FTH1 in skeletal muscle results in muscle atrophy and impaired exercise endurance. In vitro studies using FTH1 cKO myoblasts revealed notable decreases in GSH concentrations, elevated levels of lipid peroxidation, and the substantial accumulation of Fe2+, collectively implying the induction of ferroptosis. Mechanistically, E3 ubiquitin-protein ligase SMURF1 (SMURF1) acts as an E3 ubiquitin ligase for FTH1, thereby facilitating the ubiquitination and subsequent degradation of FTH1. Consequently, this activation of the ferroptosis pathway by SMURF1 impedes myoblast differentiation into myotubes. This study identifies FTH1 as a novel regulator of muscle cell differentiation and skeletal muscle development, implicating its potential significance in maintaining skeletal muscle health through the regulation of iron homeostasis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Skeletal Muscle Metabolism)
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