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Redox Control of Cardiac and Skeletal Muscle Function

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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 2020) | Viewed by 25453

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Special Issue Editor

Dr. Ashley J. Smuder

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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. The critical balance between ROS production and the antioxidant defense system regulates oxidative stress within the striated muscles. Equilibrium within the redox system is necessary to control the activation of signalling pathways that are essential for the maintenance of cardiac and skeletal muscle function. Conversely, oxidation may also 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 signalling pathways that 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 Special Issue aims to highlight original research and review articles that provide insight into understanding the role that ROS and protein oxidation play as an integral component of muscle protein breakdown and adaptation in conditions that promote cardiac and skeletal muscle dysfunction.

Sincerely,

Dr. Ashley J. Smuder
Guest Editor

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Keywords

Cardiac dysfunction
Skeletal muscle atrophy and dysfunction
Oxidative stress
Antioxidant
Proteolysis
Muscle contraction
Mitochondrial dysfunction
Disease
Inactivity
Exercise

Published Papers (6 papers)

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Research

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18 pages, 5014 KiB

Open AccessArticle

Lasting Effects of Low to Non-Lethal Radiation Exposure during Late Gestation on Offspring’s Cardiac Metabolism and Oxidative Stress

by Ashley S. Nemec-Bakk, Sarah Niccoli, Caitlund Davidson, Danika Roy, Lisa Stoa, Shayenthiran Sreetharan, Alain Simard, Douglas R. Boreham, Joanna Y. Wilson, T.C. Tai, Simon J. Lees and Neelam Khaper

Antioxidants 2021, 10(5), 816; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050816 - 20 May 2021

Cited by 5 | Viewed by 2541

Abstract

Ionizing radiation (IR) is known to cause fetal programming, but the physiological effects of low-dose IR are not fully understood. This study examined the effect of low (50 mGy) to non-lethal (300 and 1000 mGy) radiation exposure during late gestation on cardiac metabolism and oxidative stress in adult offspring. Pregnant C57BL/6J mice were exposed to 50, 300, or 1000 mGy of gamma radiation or Sham irradiation on gestational day 15. Sixteen weeks after birth, ¹⁸F-Fluorodeoxyglucose (FDG) uptake was examined in the offspring using Positron Emission Tomography imaging. Western blot was used to determine changes in oxidative stress, antioxidants, and insulin signaling related proteins. Male and female offspring from irradiated dams had lower body weights when compared to the Sham. 1000 mGy female offspring demonstrated a significant increase in ¹⁸F-FDG uptake, glycogen content, and oxidative stress. 300 and 1000 mGy female mice exhibited increased superoxide dismutase activity, decreased glutathione peroxidase activity, and decreased reduced/oxidized glutathione ratio. We conclude that non-lethal radiation during late gestation can alter glucose uptake and increase oxidative stress in female offspring. These data provide evidence that low doses of IR during the third trimester are not harmful but higher, non-lethal doses can alter cardiac metabolism later in life and sex may have a role in fetal programming. Full article

(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function)

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20 pages, 3288 KiB

Open AccessArticle

Oxidative Stress Mediates the Fetal Programming of Hypertension by Glucocorticoids

by Jeremy Lamothe, Sandhya Khurana, Sujeenthar Tharmalingam, Chad Williamson, Collin J. Byrne, Simon J. Lees, Neelam Khaper, Aseem Kumar and T.C. Tai

Antioxidants 2021, 10(4), 531; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10040531 - 29 Mar 2021

Cited by 22 | Viewed by 2887

Abstract

The field of cardiovascular fetal programming has emphasized the importance of the uterine environment on postnatal cardiovascular health. Studies have linked increased fetal glucocorticoid exposure, either from exogenous sources (such as dexamethasone (Dex) injections), or from maternal stress, to the development of adult cardiovascular pathologies. Although the mechanisms are not fully understood, alterations in gene expression driven by altered oxidative stress and epigenetic pathways are implicated in glucocorticoid-mediated cardiovascular programming. Antioxidants, such as the naturally occurring polyphenol epigallocatechin gallate (EGCG), or the superoxide dismutase (SOD) 4-hydroxy-TEMPO (TEMPOL), have shown promise in the prevention of cardiovascular dysfunction and programming. This study investigated maternal antioxidant administration with EGCG or TEMPOL and their ability to attenuate the fetal programming of hypertension via Dex injections in WKY rats. Results from this study indicate that, while Dex-programming increased blood pressure in male and female adult offspring, administration of EGCG or TEMPOL via maternal drinking water attenuated Dex-programmed increases in blood pressure, as well as changes in adrenal mRNA and protein levels of catecholamine biosynthetic enzymes phenylalanine hydroxylase (PAH), tyrosine hydroxylase (TH), dopamine beta hydroxylase (DBH), and phenylethanolamine N-methyltransferase (PNMT), in a sex-specific manner. Furthermore, programmed male offspring displayed reduced antioxidant glutathione peroxidase 1 (Gpx1) expression, increased superoxide dismutase 1 (SOD1) and catalase (CAT) expression, and increased pro-oxidant NADPH oxidase activator 1 (Noxa1) expression in the adrenal glands. In addition, prenatal Dex exposure alters expression of epigenetic regulators histone deacetylase (HDAC) 1, 5, 6, 7, 11, in male and HDAC7 in female offspring. These results suggest that glucocorticoids may mediate the fetal programming of hypertension via alteration of epigenetic machinery and oxidative stress pathways. Full article

(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function)

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13 pages, 2485 KiB

Open AccessArticle

Effects of Resistance Training on the Redox Status of Skeletal Muscle in Older Adults

by Paulo H. C. Mesquita, Donald A. Lamb, Joshua S. Godwin, Shelby C. Osburn, Bradley A. Ruple, Johnathon H. Moore, Christopher G. Vann, Kevin W. Huggins, Andrew D. Fruge, Kaelin C. Young, Andreas N. Kavazis and Michael D. Roberts

Antioxidants 2021, 10(3), 350; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030350 - 26 Feb 2021

Cited by 11 | Viewed by 2945

Abstract

The aim of this study was to investigate the effects of resistance training (RT) on the redox status of skeletal muscle in older adults. Thirteen males aged 64 ± 9 years performed full-body RT 2x/week for 6 weeks. Muscle biopsies were obtained from the vastus lateralis prior to and following RT. The mRNA, protein, and enzymatic activity levels of various endogenous antioxidants were determined. In addition, skeletal muscle 4-hydroxynonenal and protein carbonyls were determined as markers of oxidative damage. Protein levels of heat shock proteins (HSPs) were also quantified. RT increased mRNA levels of all assayed antioxidant genes, albeit protein levels either did not change or decreased. RT increased total antioxidant capacity, catalase, and glutathione reductase activities, and decreased glutathione peroxidase activity. Lipid peroxidation also decreased and HSP60 protein increased following RT. In summary, 6 weeks of RT decreased oxidative damage and increased antioxidant enzyme activities. Our results suggest the older adult responses to RT involve multi-level (transcriptional, post-transcriptional, and post-translational) control of the redox status of skeletal muscle. Full article

(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function)

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Review

Jump to: Research

26 pages, 3586 KiB

Open AccessReview

Regulation of Cardiac PKA Signaling by cAMP and Oxidants

by Friederike Cuello, Friedrich W. Herberg, Konstantina Stathopoulou, Philipp Henning and Simon Diering

Antioxidants 2021, 10(5), 663; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050663 - 24 Apr 2021

Cited by 7 | Viewed by 2925

Abstract

Pathologies, such as cancer, inflammatory and cardiac diseases are commonly associated with long-term increased production and release of reactive oxygen species referred to as oxidative stress. Thereby, protein oxidation conveys protein dysfunction and contributes to disease progression. Importantly, trials to scavenge oxidants by systemic antioxidant therapy failed. This observation supports the notion that oxidants are indispensable physiological signaling molecules that induce oxidative post-translational modifications in target proteins. In cardiac myocytes, the main driver of cardiac contractility is the activation of the β-adrenoceptor-signaling cascade leading to increased cellular cAMP production and activation of its main effector, the cAMP-dependent protein kinase (PKA). PKA-mediated phosphorylation of substrate proteins that are involved in excitation-contraction coupling are responsible for the observed positive inotropic and lusitropic effects. PKA-actions are counteracted by cellular protein phosphatases (PP) that dephosphorylate substrate proteins and thus allow the termination of PKA-signaling. Both, kinase and phosphatase are redox-sensitive and susceptible to oxidation on critical cysteine residues. Thereby, oxidation of the regulatory PKA and PP subunits is considered to regulate subcellular kinase and phosphatase localization, while intradisulfide formation of the catalytic subunits negatively impacts on catalytic activity with direct consequences on substrate (de)phosphorylation and cardiac contractile function. This review article attempts to incorporate the current perception of the functionally relevant regulation of cardiac contractility by classical cAMP-dependent signaling with the contribution of oxidant modification. Full article

(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function)

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21 pages, 3598 KiB

Open AccessFeature PaperReview

Exercise-Stimulated ROS Sensitive Signaling Pathways in Skeletal Muscle

by Jessica Bouviere, Rodrigo S. Fortunato, Corinne Dupuy, Joao Pedro Werneck-de-Castro, Denise P. Carvalho and Ruy A. Louzada

Antioxidants 2021, 10(4), 537; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10040537 - 30 Mar 2021

Cited by 74 | Viewed by 10734

Abstract

Physical exercise represents a major challenge to whole-body homeostasis, provoking acute and adaptative responses at the cellular and systemic levels. Different sources of reactive oxygen species (ROS) have been described in skeletal muscle (e.g., NADPH oxidases, xanthine oxidase, and mitochondria) and are closely related to the physiological changes induced by physical exercise through the modulation of several signaling pathways. Many signaling pathways that are regulated by exercise-induced ROS generation, such as adenosine monophosphate-activated protein kinase (AMPK), mitogen activated protein kinase (MAPK), nuclear respiratory factor2 (NRF2), and PGC-1α are involved in skeletal muscle responses to physical exercise, such as increased glucose uptake, mitochondriogenesis, and hypertrophy, among others. Most of these adaptations are blunted by antioxidants, revealing the crucial role played by ROS during and after physical exercise. When ROS generation is either insufficient or exacerbated, ROS-mediated signaling is disrupted, as well as physical exercise adaptations. Thus, an understanding the limit between “ROS that can promote beneficial effects” and “ROS that can promote harmful effects” is a challenging question in exercise biology. The identification of new mediators that cause reductive stress and thereby disrupt exercise-stimulated ROS signaling is a trending on this topic and are covered in this current review. Full article

(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function)

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20 pages, 1416 KiB

Open AccessReview

Consideration of Sex as a Biological Variable in the Development of Doxorubicin Myotoxicity and the Efficacy of Exercise as a Therapeutic Intervention

by Ryan N. Montalvo, Vivian Doerr, Branden L. Nguyen, Rachel C. Kelley and Ashley J. Smuder

Antioxidants 2021, 10(3), 343; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030343 - 25 Feb 2021

Cited by 8 | Viewed by 2694

Abstract

Doxorubicin (DOX) is an anthracycline antibiotic used to treat a wide variety of hematological and solid tumor cancers. While DOX is highly effective at reducing tumor burden, its clinical use is limited by the development of adverse effects to both cardiac and skeletal muscle. The detrimental effects of DOX to muscle tissue are associated with the increased incidence of heart failure, dyspnea, exercise intolerance, and reduced quality of life, which have been reported in both patients actively receiving chemotherapy and cancer survivors. A variety of factors elevate the probability of DOX-related morbidity in patients; however, the role of sex as a biological variable to calculate patient risk remains unclear. Uncertainty regarding sexual dimorphism in the presentation of DOX myotoxicity stems from inadequate study design to address this issue. Currently, the majority of clinical data on DOX myotoxicity come from studies where the ratio of males to females is unbalanced, one sex is omitted, and/or the patient cohort include a broad age range. Furthermore, lack of consensus on standard outcome measures, difficulties in long-term evaluation of patient outcomes, and other confounding factors (i.e., cancer type, drug combinations, adjuvant therapies, etc.) preclude a definitive answer as to whether differences exist in the incidence of DOX myotoxicity between sexes. This review summarizes the current clinical and preclinical literature relevant to sex differences in the incidence and severity of DOX myotoxicity, the proposed mechanisms for DOX sexual dimorphism, and the potential for exercise training to serve as an effective therapeutic countermeasure to preserve muscle strength and function in males and females. Full article

(This article belongs to the Special Issue Redox Control of Cardiac and Skeletal Muscle Function)

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