Mitochondrial redox potential during contraction in single intact muscle fibers

Michaelson, Luke; Shi, Guoli; Ward, Chris W.; Rodney, George G.

doi:10.1002/mus.21724

Cited by 68 publications

(65 citation statements)

References 40 publications

(48 reference statements)

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“…It is now thought that little superoxide is contributed by the mitochiondria during steady-state contractions [see Powers and Jackson (52) for review]. This estimate is in line with our recent finding that the redox state of the mitochondria (a surrogate measure of ROS generation) is unchanged during steady-state contractions (47) as well as with recent direct measures of ROS within the mitochondria of contractile muscle fibers (61).…”

Section: Mitochondriasupporting

confidence: 84%

Mechanical Stretch-Induced Activation of ROS/RNS Signaling in Striated Muscle

Ward

Prosser²,

Lederer³

2014

Antioxidants & Redox Signaling

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Significance: Mechanical activation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) occurs in striated muscle and affects Ca 2+ signaling and contractile function. ROS/RNS signaling is tightly controlled, spatially compartmentalized, and source specific. Recent Advances: Here, we review the evidence that within the contracting myocyte, the trans-membrane protein NADPH oxidase 2 (Nox2) is the primary source of ROS generated during contraction. We also review a newly characterized signaling cascade in cardiac and skeletal muscle in which the microtubule network acts as a mechanotransduction element that activates Nox2-dependent ROS generation during mechanical stretch, a pathway termed X-ROS signaling. Critical Issues: In the heart, X-ROS acts locally and affects the sarcoplasmic reticulum (SR) Ca 2+ release channels (ryanodine receptors) and tunes Ca 2+ signaling during physiological behavior, but excessive X-ROS can promote Ca 2+ -dependent arrhythmias in pathology. In skeletal muscle, X-ROS sensitizes Ca 2+ -permeable sarcolemmal ''transient receptor potential'' channels, a pathway that is critical for sustaining SR load during repetitive contractions, but when in excess, it is maladaptive in diseases such as Duchenne Musclar dystrophy. Future Directions: New advances in ROS/RNS detection as well as molecular manipulation of signaling pathways will provide critical new mechanistic insights into the details of X-ROS signaling. These efforts will undoubtedly reveal new avenues for therapeutic intervention in the numerous diseases of striated muscle in which altered mechanoactivation of ROS/RNS production has been identified. Antioxid. Redox Signal. 20,[929][930][931][932][933][934][935][936]

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Section: Mitochondriasupporting

confidence: 84%

Mechanical Stretch-Induced Activation of ROS/RNS Signaling in Striated Muscle

Ward

Prosser²,

Lederer³

2014

Antioxidants & Redox Signaling

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“…In skeletal muscle cells, NOX isoforms 2 and 4 are found at the plasma membrane, transverse tubules, and sarcoplasmic reticulum where they modulate calcium release (261). They are described as the major source of ROS during skeletal muscle contraction (217). In this context, pharmacological inhibition of NOX-induced ROS production has been widely used, although these inhibitors are mainly unspecific and not isoform selective [review in Refs.…”

Section: Fig 8 Intracellular Sources Of Ros Andmentioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

148

120

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Skeletal muscle shows high plasticity in response to external demand. Moreover, adult skeletal muscle is capable of complete regeneration after injury, due to the properties of muscle stem cells (MuSCs), the satellite cells, which follow a tightly regulated myogenic program to generate both new myofibers and new MuSCs for further needs. Although reactive oxygen species (ROS) and reactive nitrogen species (RNS) have long been associated with skeletal muscle physiology, their implication in the cell and molecular processes at work during muscle regeneration is more recent. This review focuses on redox regulation during skeletal muscle regeneration. An overview of the basics of ROS/RNS and antioxidant chemistry and biology occurring in skeletal muscle is first provided. Then, the comprehensive knowledge on redox regulation of MuSCs and their surrounding cell partners (macrophages, endothelial cells) during skeletal muscle regeneration is presented in normal muscle and in specific physiological (exercise-induced muscle damage, aging) and pathological (muscular dystrophies) contexts. Recent advances in the comprehension of these processes has led to the development of therapeutic assays using antioxidant supplementation, which result in inconsistent efficiency, underlying the need for new tools that are aimed at precisely deciphering and targeting ROS networks. This review should provide an overall insight of the redox regulation of skeletal muscle regeneration while highlighting the limits of the use of nonspecific antioxidants to improve muscle function. Antioxid. Redox Signal. 27, 276-310.

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“…A network of endogenous antioxidants acts to scavenge these ROS, but an excess intake of exogenous antioxidants might impair exercise adaptations (refer to the text for a detailed discussion apocynin, or in isolated muscle fibres with NOX inhibitors such as diphenyleneiodonium chloride, apocynin, or a specific peptide inhibitor of NOX, gp91ds-tat, completely prevents the electrically stimulated increase in ROS. 56,59,60 Nitric oxide synthase The free radical, nitric oxide (NO), is produced in the skeletal muscle fibres during contraction 59 from the neuronal NOS isoform. 61 Furthermore, the highly reactive ROS peroxynitrite (ONOO − ) is produced from the reaction of NO with ·O 2 − .…”

Section: Nadph Oxidasementioning

confidence: 99%

Skeletal muscle reactive oxygen species: A target of good cop/bad cop for exercise and disease

Mason

Wadley

2014

Redox Report

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Metabolic stresses associated with disease, ageing, and exercise increase the levels of reactive oxygen species (ROS) in skeletal muscle. These ROS have been linked mechanistically to adaptations in skeletal muscle that can be favourable (i.e. in response to exercise) or detrimental (i.e. in response to disease). The magnitude, duration (acute versus chronic), and cellular origin of the ROS are important underlying factors in determining the metabolic perturbations associated with the ROS produced in skeletal muscle. In particular, insulin resistance has been linked to excess ROS production in skeletal muscle mitochondria. A chronic excess of mitochondrial ROS can impair normal insulin signalling pathways and glucose disposal in skeletal muscle. In contrast, ROS produced in skeletal muscle in response to exercise has been linked to beneficial metabolic adaptations including mitochondrial biogenesis and muscle hypertrophy. Moreover, unlike insulin resistance, exercise-induced ROS appears to be primarily of nonmitochondrial origin. The present review summarizes the diverse ROS-targeted metabolic outcomes associated with insulin resistance versus exercise in skeletal muscle, thus, presenting two contrasting perspectives of pathologically harmful versus physiologically beneficial ROS. Here, we discuss the key sites of ROS production during exercise and the effect of ROS in skeletal muscle of people with type 2 diabetes.

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Mitochondrial redox potential during contraction in single intact muscle fibers

Cited by 68 publications

References 40 publications

Mechanical Stretch-Induced Activation of ROS/RNS Signaling in Striated Muscle

Mechanical Stretch-Induced Activation of ROS/RNS Signaling in Striated Muscle

Redox Control of Skeletal Muscle Regeneration

Skeletal muscle reactive oxygen species: A target of good cop/bad cop for exercise and disease

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