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Antioxidants
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Redox Control of Cardiac and Skeletal Muscle Function II
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Redox Control of Cardiac and Skeletal Muscle Function II

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 (30 November 2022) | Viewed by 14451

Special Issue Editor

Dr. Ashley J. Smuder

E-Mail Website
Guest Editor
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA
Interests: cancer and chemotherapy; cardiac and skeletal muscle; mitochondrial dysfunction; redox balance and exercise
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The supraphysiological production of reactive oxygen species (ROS) in cardiac and skeletal muscle is a hallmark of numerous conditions associated with muscle contractile dysfunction, including but not limited to disease, inactivity, and aging. Equilibrium within the redox system is necessary to control the activation of signaling pathways, which are essential for the maintenance of cardiac and skeletal muscle function. Conversely, oxidation may lead to changes in protein activities that promote beneficial adaptations in gene expression. Thus, a more comprehensive understanding of the mechanisms by which altered redox regulation can modulate signaling pathways, which, in turn, regulate muscle contractile protein function, is needed to develop therapeutic interventions to prevent cardiac and skeletal muscle dysfunction resulting from a diverse array of conditions.

This second edition Special Issue welcomes manuscripts that could fill the gap between mechanistic understanding of redox signaling and utilization of antioxidative therapies as they relate to disease and wasting conditions. This issue includes but is not limited to the following themes:

  • Redox control of cardiac and skeletal muscle atrophy and/or dysfunction;
  • Use of antioxidative drugs to counteract cardiac and skeletal muscle atrophy and/or dysfunction;
  • Emerging antioxidant therapies;
  • Novel mechanisms regulating redox signaling;
  • Exercise and its effect on redox balance in cardiac and skeletal muscle.

Dr. Ashley J. Smuder
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.

Published Papers (4 papers)

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Research

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14 pages, 2966 KiB  
Article
Effects of Hyperbaric Oxygen Preconditioning on Doxorubicin Cardiorespiratory Toxicity
by Vivian Doerr, Ryan N. Montalvo, Branden L. Nguyen, Franccesco P. Boeno, Michael D. Sunshine, Victoria E. Bindi, David D. Fuller and Ashley J. Smuder
Antioxidants 2022, 11(10), 2073; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11102073 - 20 Oct 2022
Cited by 1 | Viewed by 1927
Abstract
Cardiorespiratory dysfunction resulting from doxorubicin (DOX) chemotherapy treatment is a debilitating condition affecting cancer patient outcomes and quality of life. DOX treatment promotes cardiac and respiratory muscle pathology due to enhanced reactive oxygen species (ROS) production, mitochondrial dysfunction and impaired muscle contractility. In [...] Read more.
Cardiorespiratory dysfunction resulting from doxorubicin (DOX) chemotherapy treatment is a debilitating condition affecting cancer patient outcomes and quality of life. DOX treatment promotes cardiac and respiratory muscle pathology due to enhanced reactive oxygen species (ROS) production, mitochondrial dysfunction and impaired muscle contractility. In contrast, hyperbaric oxygen (HBO) therapy is considered a controlled oxidative stress that can evoke a substantial and sustained increase in muscle antioxidant expression. This HBO-induced increase in antioxidant capacity has the potential to improve cardiac and respiratory (i.e., diaphragm) muscle redox balance, preserving mitochondrial function and preventing muscle dysfunction. Therefore, we determined whether HBO therapy prior to DOX treatment is sufficient to enhance muscle antioxidant expression and preserve muscle redox balance and cardiorespiratory muscle function. To test this, adult female Sprague Dawley rats received HBO therapy (2 or 3 atmospheres absolute (ATA), 100% O2, 1 h/day) for 5 consecutive days prior to acute DOX treatment (20 mg/kg i.p.). Our data demonstrate that 3 ATA HBO elicits a greater antioxidant response compared to 2 ATA HBO. However, these effects did not correspond with beneficial adaptations to cardiac systolic and diastolic function or diaphragm muscle force production in DOX treated rats. These findings suggest that modulating muscle antioxidant expression with HBO therapy is not sufficient to prevent DOX-induced cardiorespiratory dysfunction. Full article
(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function II)
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17 pages, 4137 KiB  
Article
Addition of oh8dG to Cardioplegia Attenuated Myocardial Oxidative Injury through the Inhibition of Sodium Bicarbonate Cotransporter Activity
by Min Jeong Ji, Kuk Hui Son and Jeong Hee Hong
Antioxidants 2022, 11(9), 1641; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11091641 - 24 Aug 2022
Cited by 3 | Viewed by 1311
Abstract
The biomarker 8-hydroxy-2′-deoxyguanosine (oh8dG) is derived from oxidized nucleic acids or products of oxidant-mediated DNA damage. Enhanced sodium bicarbonate cotransporter (NBC) activity is caused by reactive oxygen species (ROS) production in ventricular myocytes. Thus, we hypothesized that cardioplegia-solution-mediated ROS generation may be involved [...] Read more.
The biomarker 8-hydroxy-2′-deoxyguanosine (oh8dG) is derived from oxidized nucleic acids or products of oxidant-mediated DNA damage. Enhanced sodium bicarbonate cotransporter (NBC) activity is caused by reactive oxygen species (ROS) production in ventricular myocytes. Thus, we hypothesized that cardioplegia-solution-mediated ROS generation may be involved in the regulation of NBC activity in cardiomyocytes and that oh8dG treatment may modulate ROS and associated NBC activity. Langendorff-free cardioplegia-arrested cardiac strips and cardiomyocytes were isolated to determine the NBC activity and effects of oh8dG on oxidative-stress-mediated cardiac damage markers. We first determined the histidine-tryptophan-ketoglutarate (HTK) solution mediated NBC activity in cardiac strips and cells. The oh8dG treatment attenuated NBC activity in the electroneutral or electrogenic form of NBC. Additionally, exposure to HTK solution induced ROS, whereas co-administration of oh8dG attenuated ROS-mediated NBC activity, reduced ROS levels, and decreased the expression of apoptotic markers and fibrosis-associated proteins in cardiac cells. The oh8dG-administrated cardiac tissues were also protected from enhanced HTK-induced damage markers, heat shock protein 60 and polyADP-ribose. Our results show that oh8dG has a protective role against myocardial oxidative damage and provides a useful treatment strategy for restoring cardiac function. Full article
(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function II)
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14 pages, 1104 KiB  
Article
Effects of the SGLT2 Inhibition on Cardiac Remodeling in Streptozotocin-Induced Diabetic Rats, a Model of Type 1 Diabetes Mellitus
by Camila Moreno Rosa, Dijon Henrique Salome Campos, David Rafael Abreu Reyes, Felipe Cesar Damatto, Lucas Yamada Kurosaki, Luana Urbano Pagan, Mariana Janini Gomes, Camila Renata Corrêa, Ana Angelica Henrique Fernandes, Marina Politi Okoshi and Katashi Okoshi
Antioxidants 2022, 11(5), 982; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050982 - 17 May 2022
Cited by 7 | Viewed by 2109
Abstract
Clinical trials have shown that sodium glucose co-transporter 2 (SGLT2) inhibitors improve clinical outcomes in diabetes mellitus (DM) patients. As most studies were performed in Type 2 DM, the cardiovascular effects of SGLT2 inhibition still require clarification in Type 1 DM. We analyzed [...] Read more.
Clinical trials have shown that sodium glucose co-transporter 2 (SGLT2) inhibitors improve clinical outcomes in diabetes mellitus (DM) patients. As most studies were performed in Type 2 DM, the cardiovascular effects of SGLT2 inhibition still require clarification in Type 1 DM. We analyzed the effects of SGLT2 inhibitor dapagliflozin on cardiac remodeling in rats with streptozotocin-induced diabetes, an experimental model of Type 1 DM. Methods: Male Wistar rats were assigned into four groups: control (C, n = 14); control treated with dapagliflozin (C + DAPA, n = 14); diabetes (DM, n = 20); and diabetes treated with dapagliflozin (DM + DAPA, n = 20) for 8 weeks. Dapagliflozin dosage was 5 mg/kg/day. Statistical analyses: ANOVA and Tukey or Kruskal–Wallis and Dunn. Results: DM + DAPA presented decreased blood pressure and glycemia and increased body weight compared to DM (C 507 ± 52; C + DAPA 474 ± 50; DM 381 ± 52 *; DM + DAPA 430 ± 48 # g; * p < 0.05 vs. C; # p < 0.05 vs. C + DAPA and DM + DAPA). DM echocardiogram presented left ventricular and left atrium dilation with impaired systolic and diastolic function. Cardiac changes were attenuated by dapagliflozin. Myocardial hydroxyproline concentration and interstitial collagen fraction did not differ between groups. The expression of Type III collagen was lower in DM and DM + DAPA than their controls. Type I collagen expression and Type I-to-III collagen ratio were lower in DM + DAPA than C + DAPA. DM + DAPA had lower lipid hydroperoxide concentration (C 275 ± 42; C + DAPA 299 ± 50; DM 385 ± 54 *; DM + DAPA 304 ± 40 # nmol/g tissue; * p < 0.05 vs. C; # p < 0.05 vs. DM) and higher superoxide dismutase and glutathione peroxidase activity than DM. Advanced glycation end products did not differ between groups. Conclusion: Dapagliflozin is safe, increases body weight, decreases glycemia and oxidative stress, and attenuates cardiac remodeling in an experimental rat model of Type 1 diabetes mellitus. Full article
(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function II)
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Review

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14 pages, 1718 KiB  
Review
Exercise Training and Skeletal Muscle Antioxidant Enzymes: An Update
by Scott K. Powers, Erica Goldstein, Matthew Schrager and Li Li Ji
Antioxidants 2023, 12(1), 39; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12010039 - 25 Dec 2022
Cited by 26 | Viewed by 8425
Abstract
The pivotal observation that muscular exercise is associated with oxidative stress in humans was first reported over 45 years ago. Soon after this landmark finding, it was discovered that contracting skeletal muscles produce oxygen radicals and other reactive species capable of oxidizing cellular [...] Read more.
The pivotal observation that muscular exercise is associated with oxidative stress in humans was first reported over 45 years ago. Soon after this landmark finding, it was discovered that contracting skeletal muscles produce oxygen radicals and other reactive species capable of oxidizing cellular biomolecules. Importantly, the failure to eliminate these oxidant molecules during exercise results in oxidation of cellular proteins and lipids. Fortuitously, muscle fibers and other cells contain endogenous antioxidant enzymes capable of eliminating oxidants. Moreover, it is now established that several modes of exercise training (e.g., resistance exercise and endurance exercise) increase the expression of numerous antioxidant enzymes that protect myocytes against exercise-induced oxidative damage. This review concisely summarizes the impact of endurance, high-intensity interval, and resistance exercise training on the activities of enzymatic antioxidants within skeletal muscles in humans and other mammals. We also discuss the evidence that exercise-induced up-regulation of cellular antioxidants reduces contraction-induced oxidative damage in skeletal muscles and has the potential to delay muscle fatigue and improve exercise performance. Finally, in hopes of stimulating further research, we also discuss gaps in our knowledge of exercise-induced changes in muscle antioxidant capacity. Full article
(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function II)
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