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Antioxidants
Special Issues
Mitochondrial Function, Reactive Oxygen/Nitrogen Species and Skeletal Muscle
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Mitochondrial Function, Reactive Oxygen/Nitrogen Species and Skeletal Muscle

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: closed (15 October 2021) | Viewed by 8972

Special Issue Editors

Prof. Dr. Håkan Westerblad

E-Mail Website
Guest Editor
Karolinska Institutet, Stockholm, Sweden
Interests: muscle fatigue; muscle weakness; endurance training; cellular Ca2+-handling; reactive oxygen/nitrogen species; mitochondrial myopahies; inflammatory myopathies
Dr. Takashi Yamada

E-Mail Website
Guest Editor
Department of Physical Therapy, Sapporo Medical University, Sapporo, Japan
Interests: sarcopenia; cachexia; inflammatory myopathies; muscular dystrophy; muscle strength; muscle weakness; mechanical stress; oxidative/nitrative stress; excitation-contraction coupling; myofibril

Special Issue Information

Dear Colleagues,

Mitochondria have a key role in the handling of reactive oxygen/nitrogen species (RONS) in skeletal muscle. Traditionally, increased production of RONS has been linked to oxidative stress, resulting in impaired contractility and muscle atrophy. However, recent research has revealed important physiological signaling roles of RONS in skeletal muscle; for instance, transiently increased RONS production is involved in the triggering of beneficial adaptations in response to endurance exercise. 

In this Special Issue, we aim to collect experimental research studies addressing mechanisms underlying the interactions between mitochondrial function and RONS in skeletal muscle. We welcome papers dealing with prolonged alterations in mitochondria–RONS interactions, which are generally linked to deleterious effects in muscle, as well as with transient alterations, which might trigger beneficial adaptations. 

Prof. Dr. Håkan Westerblad
Dr. Takashi Yamada
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 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

  • Mechanisms: molecular, physiological, and pathological
  • Muscle contraction
  • Physical exercise
  • Muscle disease
  • Reactive Oxygen Species
  • ROS
  • Reactive Nitrogen Species
  • RNS

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Published Papers (3 papers)

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Research

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28 pages, 7759 KiB  
Article
SKP-SC-EVs Mitigate Denervated Muscle Atrophy by Inhibiting Oxidative Stress and Inflammation and Improving Microcirculation
by Wei Wang, Dingding Shen, Lilei Zhang, Yanan Ji, Lai Xu, Zehao Chen, Yuntian Shen, Leilei Gong, Qi Zhang, Mi Shen, Xiaosong Gu and Hualin Sun
Antioxidants 2022, 11(1), 66; https://doi.org/10.3390/antiox11010066 - 28 Dec 2021
Cited by 23 | Viewed by 3088
Abstract
Denervated muscle atrophy is a common clinical disease that has no effective treatments. Our previous studies have found that oxidative stress and inflammation play an important role in the process of denervated muscle atrophy. Extracellular vesicles derived from skin precursor-derived Schwann cells (SKP-SC-EVs) [...] Read more.
Denervated muscle atrophy is a common clinical disease that has no effective treatments. Our previous studies have found that oxidative stress and inflammation play an important role in the process of denervated muscle atrophy. Extracellular vesicles derived from skin precursor-derived Schwann cells (SKP-SC-EVs) contain a large amount of antioxidants and anti-inflammatory factors. This study explored whether SKP-SC-EVs alleviate denervated muscle atrophy by inhibiting oxidative stress and inflammation. In vitro studies have found that SKP-SC-EVs can be internalized and caught by myoblasts to promote the proliferation and differentiation of myoblasts. Nutrient deprivation can cause myotube atrophy, accompanied by oxidative stress and inflammation. However, SKP-SC-EVs can inhibit oxidative stress and inflammation caused by nutritional deprivation and subsequently relieve myotube atrophy. Moreover, there is a remarkable dose-effect relationship. In vivo studies have found that SKP-SC-EVs can significantly inhibit a denervation-induced decrease in the wet weight ratio and myofiber cross-sectional area of target muscles. Furthermore, SKP-SC-EVs can dramatically inhibit highly expressed Muscle RING Finger 1 and Muscle Atrophy F-box in target muscles under denervation and reduce the degradation of the myotube heavy chain. SKP-SC-EVs may reduce mitochondrial vacuolar degeneration and autophagy in denervated muscles by inhibiting autophagy-related proteins (i.e., PINK1, BNIP3, LC3B, and ATG7). Moreover, SKP-SC-EVs may improve microvessels and blood perfusion in denervated skeletal muscles by enhancing the proliferation of vascular endothelial cells. SKP-SC-EVs can also significantly inhibit the production of reactive oxygen species (ROS) in target muscles after denervation, which indicates that SKP-SC-EVs elicit their role by upregulating Nrf2 and downregulating ROS production-related factors (Nox2 and Nox4). In addition, SKP-SC-EVs can significantly reduce the levels of interleukin 1β, interleukin-6, and tumor necrosis factor α in target muscles. To conclude, SKP-SC-EVs may alleviate the decrease of target muscle blood perfusion and passivate the activities of ubiquitin-proteasome and autophagy-lysosome systems by inhibiting oxidative stress and inflammatory response, then reduce skeletal muscle atrophy caused by denervation. This study not only enriches the molecular regulation mechanism of denervated muscle atrophy, but also provides a scientific basis for SKP-SC-EVs as a protective drug to prevent and treat muscle atrophy. Full article
(This article belongs to the Special Issue Mitochondrial Function, Reactive Oxygen/Nitrogen Species and Skeletal Muscle)
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12 pages, 1467 KiB  
Article
Vitamin C and E Treatment Blocks Changes in Kynurenine Metabolism Triggered by Three Weeks of Sprint Interval Training in Recreationally Active Elderly Humans
by Victoria L. Wyckelsma, Ada Trepci, Lilly Schwieler, Tomas Venckunas, Marius Brazaitis, Sigitas Kamandulis, Henrikas Paulauskas, Helena Gapeyeva, Mati Pääsuke, Stefano Gastaldello, Sophie Imbeault, Håkan Westerblad, Sophie Erhardt and Daniel C. Andersson
Antioxidants 2021, 10(9), 1443; https://doi.org/10.3390/antiox10091443 - 10 Sep 2021
Cited by 2 | Viewed by 2607
Abstract
The kynurenine pathway (KP) is gaining attention in several clinical fields. Recent studies show that physical exercise offers a therapeutic way to improve ratios of neurotoxic to neuroprotective KP metabolites. Antioxidant supplementation can blunt beneficial responses to physical exercise. We here studied the [...] Read more.
The kynurenine pathway (KP) is gaining attention in several clinical fields. Recent studies show that physical exercise offers a therapeutic way to improve ratios of neurotoxic to neuroprotective KP metabolites. Antioxidant supplementation can blunt beneficial responses to physical exercise. We here studied the effects of endurance training in the form of sprint interval training (SIT; three sessions of 4–6 × 30 s cycling sprints per week for three weeks) in elderly (~65 years) men exposed to either placebo (n = 9) or the antioxidants vitamin C (1 g/day) and E (235 mg/day) (n = 11). Blood samples and muscle biopsies were taken under resting conditions in association with the first (untrained state) and last (trained state) SIT sessions. In the placebo group, the blood plasma level of the neurotoxic quinolinic acid was lower (~30%) and the neuroprotective kynurenic acid to quinolinic acid ratio was higher (~50%) in the trained than in the untrained state. Moreover, muscle biopsies showed a training-induced increase in kynurenine aminotransferase (KAT) III in the placebo group. All these training effects were absent in the vitamin-treated group. In conclusion, KP metabolism was shifted towards neuroprotection after three weeks of SIT in elderly men and this shift was blocked by antioxidant treatment. Full article
(This article belongs to the Special Issue Mitochondrial Function, Reactive Oxygen/Nitrogen Species and Skeletal Muscle)
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Other

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8 pages, 251 KiB  
Perspective
The Role of Nrf2 in Skeletal Muscle on Exercise Capacity
by Yu Kitaoka
Antioxidants 2021, 10(11), 1712; https://doi.org/10.3390/antiox10111712 - 27 Oct 2021
Cited by 21 | Viewed by 2606
Abstract
Nuclear factor erythroid 2-related factor 2 Nfe2l2 (Nrf2) is believed to play a crucial role in protecting cells against oxidative stress. In addition to its primary function of maintaining redox homeostasis, there is emerging evidence that Nrf2 is also involved in energy metabolism. [...] Read more.
Nuclear factor erythroid 2-related factor 2 Nfe2l2 (Nrf2) is believed to play a crucial role in protecting cells against oxidative stress. In addition to its primary function of maintaining redox homeostasis, there is emerging evidence that Nrf2 is also involved in energy metabolism. In this review, we briefly discuss the role of Nrf2 in skeletal muscle metabolism from the perspective of exercise physiology. This article is part of a special issue “Mitochondrial Function, Reactive Oxygen/Nitrogen Species and Skeletal Muscle” edited by Håkan Westerblad and Takashi Yamada. Full article
(This article belongs to the Special Issue Mitochondrial Function, Reactive Oxygen/Nitrogen Species and Skeletal Muscle)
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