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Antioxidants
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Redox Regulation of Skeletal Muscle Mass and Function in Health...
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Redox Regulation of Skeletal Muscle Mass and Function in Health and Disease

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 11886

Special Issue Editor

Prof. Dr. Claudio Cabello-Verrugio

E-Mail Website
Guest Editor
Departamento de Ciencias Biológicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Santiago, Chile
Interests: primary and secondary sarcopenia; bile acids; satellite cells; fibrosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The number of people affected by non-transmissible chronic diseases and aging has increased in the last years. The critical causes of these pathological states include oxidative stress—an imbalance between the formation of oxidant species, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS)—and antioxidant mechanisms. Many tissues, including skeletal muscle, are exposed to oxidative stress with harmful biological effects of ROS, such as alteration of muscle function and physiology. ROS can regulate several redox-sensitive signaling pathways that play a critical role in gene expression or protein modification. While oxidant species have gained a great deal of attention regarding their harmful effects on muscle contractibility, fatigue, and metabolic dysfunction, research has also shown that ROS facilitate muscle adaptation after stressors such as physical exercise.

We invite researchers and scientists to contribute original research and review articles that reflect recent progress in elucidating the mechanisms in the balance between ROS and cellular antioxidant machinery. This may be altered during muscle pathologies, emphasizing aging and chronic diseases. We welcome all articles that describe new and essential findings on the role of oxidative stress in sarcopenia, cachexia, myopathies, or any other muscle dysfunction, and anticipate submissions that allow for expansion of knowledge and describe new strategies to treat or prevent a pathological status in which oxidative stress might be involved.

Dr. C Cabello-Verrugio
Guest Editor

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

  • skeletal muscle
  • oxidative stress
  • ROS
  • sarcopenia
  • cachexia
  • redox signaling

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Published Papers (4 papers)

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Research

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9 pages, 410 KiB  
Article
Serum α-Carotene, but Not Other Antioxidants, Is Positively Associated with Muscle Strength in Older Adults: NHANES 2001–2002
by Renata R. Bruno, Fernanda C. Rosa, Paula C. Nahas, Flávia M. S. de Branco and Erick P. de Oliveira
Antioxidants 2022, 11(12), 2386; https://doi.org/10.3390/antiox11122386 - 1 Dec 2022
Cited by 7 | Viewed by 3140
Abstract
Aging is associated with an increased reactive oxygen species that can decrease muscle strength. Thus, antioxidant substances could be positively associated with muscle strength in older adults. To investigate the association between serum antioxidants and muscle strength in older adults. A cross-sectional study [...] Read more.
Aging is associated with an increased reactive oxygen species that can decrease muscle strength. Thus, antioxidant substances could be positively associated with muscle strength in older adults. To investigate the association between serum antioxidants and muscle strength in older adults. A cross-sectional study evaluating 1172 individuals (627 men and 545 women), aged 50 to 85 years from NHANES 2001–2002, was performed. Carotenoids (α-carotene, trans-β-carotene, cis-β-carotene, β-cryptoxanthin, lutein/zeaxanthin combination, trans-lycopene), vitamin E, and retinol were analyzed via the high-performance liquid chromatography method. Muscle strength was evaluated by the isokinetic knee extension test. Linear regression was performed to evaluate the association between tertiles of serum antioxidant levels and strength, adjusted for confounders (energy and protein intake, body mass index, sex, age, C-reactive protein, uric acid, race/ethnicity, marital status, annual household income, educational level, physical activity, smoking, hypertension, arthritis, and diabetes). Alpha-carotene levels (p-trend = 0.027) were positively associated with muscle strength. However, serum vitamin E, trans-β-carotene, cis-β-carotene, β-cryptoxanthin, carotenoids, and retinol levels were not associated with strength. Serum α-carotene, but not other antioxidants, was positively associated with muscle strength in older adults. Full article
(This article belongs to the Special Issue Redox Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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14 pages, 3285 KiB  
Article
Acylated Ghrelin Receptor Agonist HM01 Decreases Lean Body and Muscle Mass, but Unacylated Ghrelin Protects against Redox-Dependent Sarcopenia
by Rojina Ranjit, Holly Van Remmen and Bumsoo Ahn
Antioxidants 2022, 11(12), 2358; https://doi.org/10.3390/antiox11122358 - 28 Nov 2022
Cited by 4 | Viewed by 2031
Abstract
Sarcopenia, the progressive loss of muscle mass and dysfunction, universally affects the elderly and is closely associated with frailty and reduced quality of life. Despite the inevitable consequences of sarcopenia and its relevance to healthspan, no pharmacological therapies are currently available. Ghrelin is [...] Read more.
Sarcopenia, the progressive loss of muscle mass and dysfunction, universally affects the elderly and is closely associated with frailty and reduced quality of life. Despite the inevitable consequences of sarcopenia and its relevance to healthspan, no pharmacological therapies are currently available. Ghrelin is a gut-released hormone that increases appetite and body weight upon acylation, which activates its receptor GHSR1a. Recent studies have demonstrated that acyl and unacylated ghrelin are protective against acute pathological conditions of skeletal muscle. We hypothesized that both acyl ghrelin receptor agonist (HM01) and unacylated ghrelin ameliorate muscle atrophy and contractile dysfunction in oxidative stress-induced sarcopenia. HM01, unacylated ghrelin, or saline was delivered via osmotic pump. HM01 increased food consumption transiently, while the body weight remained elevated. It also decreased lean body mass and muscle mass of wildtype and Sod1KO. In contrast, unacylated ghrelin ameliorated loss of muscle mass by 15–30% in Sod1KO mice without changes in food consumption or body weights. Contractile force was decreased by ~30% in Sod1KO mice, but unacylated ghrelin prevented the force deficit by ~80%. We identified downregulation of transcription factor FoxO3a and its downstream E3 ligase MuRF1 by unacylated ghrelin. Our data show a direct role of unacylated ghrelin in redox-dependent sarcopenia independent of changes of food consumption or body weight. Full article
(This article belongs to the Special Issue Redox Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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15 pages, 3917 KiB  
Article
Bile Acids Induce Alterations in Mitochondrial Function in Skeletal Muscle Fibers
by Johanna Abrigo, Hugo Olguín, Danae Gutierrez, Franco Tacchi, Marco Arrese, Daniel Cabrera, Mayalen Valero-Breton, Alvaro A. Elorza, Felipe Simon and Claudio Cabello-Verrugio
Antioxidants 2022, 11(9), 1706; https://doi.org/10.3390/antiox11091706 - 30 Aug 2022
Cited by 16 | Viewed by 2647
Abstract
Cholestatic chronic liver disease is characterized by developing sarcopenia and elevated serum levels of bile acids. Sarcopenia is a skeletal muscle disorder with the hallmarks of muscle weakness, muscle mass loss, and muscle strength decline. Our previous report demonstrated that deoxycholic acid (DCA) [...] Read more.
Cholestatic chronic liver disease is characterized by developing sarcopenia and elevated serum levels of bile acids. Sarcopenia is a skeletal muscle disorder with the hallmarks of muscle weakness, muscle mass loss, and muscle strength decline. Our previous report demonstrated that deoxycholic acid (DCA) and cholic acid (CA), through the membrane receptor TGR5, induce a sarcopenia-like phenotype in myotubes and muscle fibers. The present study aimed to evaluate the impact of DCA and CA on mitochondrial mass and function in muscle fibers and the role of the TGR5 receptor. To this end, muscle fibers obtained from wild-type and TGR5−/− mice were incubated with DCA and CA. Our results indicated that DCA and CA decreased mitochondrial mass, DNA, and potential in a TGR5-dependent fashion. Furthermore, with TGR5 participation, DCA and CA also reduced the oxygen consumption rate and complexes I and II from the mitochondrial electron transport chain. In addition, DCA and CA generated more mitochondrial reactive oxygen species than the control, which were abolished in TGR5−/− mice muscle fibers. Our results indicate that DCA and CA induce mitochondrial dysfunction in muscle fibers through a TGR5-dependent mechanism. Full article
(This article belongs to the Special Issue Redox Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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Review

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16 pages, 663 KiB  
Review
Resolution of Inflammation after Skeletal Muscle Ischemia–Reperfusion Injury: A Focus on the Lipid Mediators Lipoxins, Resolvins, Protectins and Maresins
by Cindy Barnig, Gaetan Lutzweiler, Margherita Giannini, Anne Lejay, Anne-Laure Charles, Alain Meyer and Bernard Geny
Antioxidants 2022, 11(6), 1213; https://doi.org/10.3390/antiox11061213 - 20 Jun 2022
Cited by 11 | Viewed by 3510
Abstract
Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation [...] Read more.
Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation can also result from defects in resolution signaling. Importantly, the resolution of inflammation is an active process also based on specific lipid mediators including lipoxins, resolvins and maresins that orchestrate the potential return to tissue homeostasis. Thus, lipid mediators have received growing attention since they dampen deleterious effects related to ischemia–reperfusion. For instance, the treatment of skeletal muscles with resolvins prior to ischemia decreases polymorphonuclear leukocyte (PMN) infiltration. Additionally, remote alterations in lungs or kidneys are reduced when enhancing lipid mediators’ functions. Accordingly, lipoxins prevented oxidative-stress-mediated tissue injuries, macrophage polarization was modified and in mice lacking DRV2 receptors, ischemia/reperfusion resulted in excessive leukocyte accumulation. In this review, we first aimed to describe the inflammatory response during ischemia and reperfusion in skeletal muscle and then discuss recent discoveries in resolution pathways. We focused on the role of specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) and their potential therapeutic applications. Full article
(This article belongs to the Special Issue Redox Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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