The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes

Kozakowska, Magdalena; Pietraszek-Gremplewicz, Katarzyna; Józkowicz, Alicja; Dulak, Józef

doi:10.1007/s10974-015-9438-9

Cited by 240 publications

(217 citation statements)

References 192 publications

(334 reference statements)

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“…Passive mechanical stretch of a muscle cell may generate ROS, which are required for proliferation and differentiation of muscle cells [Palomero et al, 2012]. Under physiological conditions, these ROS are balanced by ROS scavengers so that appropriate levels of ROS are maintained to facilitate cell proliferation [Bigarella et al, 2014;Kozakowska et al, 2015]. However, as stretching intensifies, more ROS are produced and they eventually outpace ROS scavenging, damaging many cellular components and causing adverse effects on cells.…”

Section: Discussionmentioning

confidence: 99%

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Simultaneous Study of Mechanical Stretch-Induced Cell Proliferation and Apoptosis on C2C12 Myoblasts

Feng

Tian

Sun

et al. 2018

Cells Tissues Organs

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Mechanical stretch may cause myoblasts to either proliferate or undergo apoptosis. Identifying the molecular events that switch the fate of a stretched cell from proliferation to apoptosis is practically important in the field of regenerative medicine. A recent study on vascular smooth muscle cells illustrated that identification of these events may be achieved by addressing the stretch-induced opposite cellular outcomes simultaneously within a single investigation. To define conditions or a model in which both proliferation and apoptosis can be studied at the same time, we exposed in vitro cultured C2C12 myoblasts to a cyclic mechanical stretch regimen of 15% elongation at a stretching frequency of 1 Hz for 0, 2, 4, 6, or 8 h every day, consecutively, for 3 days. Both proliferation and apoptosis were observed. Moreover, as the duration of the stretch was prolonged, cell proliferation increased until it peaked at the optimal stretching duration. Afterwards, apoptosis gradually prevailed. Therefore, we established a model in which stretch-induced cell proliferation and apoptosis can be studied simultaneously.

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Section: Discussionmentioning

confidence: 99%

“…However, as stretching intensifies, more ROS are produced and they eventually outpace ROS scavenging, damaging many cellular components and causing adverse effects on cells. Indeed, elevated cellular levels of ROS are associated with apoptosis [Cheng et al, 1995;Pimentel et al, 2001;Kozakowska, et al, 2015].…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Study of Mechanical Stretch-Induced Cell Proliferation and Apoptosis on C2C12 Myoblasts

Feng

Tian

Sun

et al. 2018

Cells Tissues Organs

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“…The increase of oxidative stress in muscular dystrophy, which was acknowledged a long time ago (132,228), has been shown to correlate with the severity of the pathology (274) and is considered to contribute to the pathology of several muscular dystrophies (173). Interestingly, mutations in the antioxidant sepn1 gene cause SEPN1-related myopathy, a different class of muscle disease (14).…”

Section: Muscular Dystrophiesmentioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

152

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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“…GRX2 is expressed in the mitochondria,165 GRX3 in the cytosolic and nuclear compartment, and monothiol GRX5 has a mitochondrial translocation signal and shares the active site motif of GRX3 166. Evidence has also shown that the GRX system can also catalyse reversible protein glutathionylation,167 which is an important redox regulatory mechanism, and control the redox state of thiol groups168 in situations where the redox environment is being compromised.…”

Section: Regulatory Reactive Oxygen and Nitrogen Species Enzymes Exprmentioning

confidence: 99%

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age‐related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ‘epidemic’ problem, the primary biochemical and molecular mechanisms underlying age‐related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age‐associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age‐related muscle atrophy and weakness.

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The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes

Cited by 240 publications

References 192 publications

Simultaneous Study of Mechanical Stretch-Induced Cell Proliferation and Apoptosis on C2C12 Myoblasts

Simultaneous Study of Mechanical Stretch-Induced Cell Proliferation and Apoptosis on C2C12 Myoblasts

Redox Control of Skeletal Muscle Regeneration

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

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