Redox modulation of muscle mass and function

Gómez-Cabrera, Mari Carmen; Arc-Chagnaud, Coralie; Salvador‐Pascual, Andrea; Brioche, Thomas; Chopard, Angèle; Olaso‐González, Gloria; Viña, José

doi:10.1016/j.redox.2020.101531

Cited by 29 publications

(29 citation statements)

References 192 publications

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“…The calpain (calcium-dependent, non-lysosomal cysteine protease) system is a calciumdependent ATP-independent pathway that cleaves myofibril proteins [13]. Calpain content and activity are known to increase with age [14], and H 2 O 2 has been shown to increase calpain 1 and 2 expression and activity in C2C12 myotubes and in human myoblasts [15,16].…”

Section: Protein Degradationmentioning

confidence: 99%

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Foreman

Hesse

2021

IJMS

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Sarcopenia, the age-related decline in muscle mass and function, derives from multiple etiological mechanisms. Accumulative research suggests that reactive oxygen species (ROS) generation plays a critical role in the development of this pathophysiological disorder. In this communication, we review the various signaling pathways that control muscle metabolic and functional integrity such as protein turnover, cell death and regeneration, inflammation, organismic damage, and metabolic functions. Although no single pathway can be identified as the most crucial factor that causes sarcopenia, age-associated dysregulation of redox signaling appears to underlie many deteriorations at physiological, subcellular, and molecular levels. Furthermore, discord of mitochondrial homeostasis with aging affects most observed problems and requires our attention. The search for the primary suspect of the fundamental mechanism for sarcopenia will likely take more intense research for the secret of this health hazard to the elderly to be unlocked.

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Section: Protein Degradationmentioning

confidence: 99%

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Foreman

Hesse

2021

IJMS

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“…Thus, we propose another potential therapy, where combinational inhibitions of mitochondrial ROS generation and mitophagy activation prevent disuse-induced muscle atrophy. The effects of antioxidants on disuse-induced muscle atrophy have been well studied in rodents and humans (Gomez-Cabrera et al, 2020). Although antioxidants, such as carotenoids and resveratrol, exhibited protective effects on animal models of muscle disuse, no antioxidant worked in human studies (Arc-Chagnaud et al, 2020;Asami et al, 2018;Jackson et al, 2010;Ogawa et al, 2013;Shibaguchi et al, 2016;Yoshihara et al, 2017).…”

Section: Mitophagy-related Gene Expression During Hindlimb Immentioning

confidence: 99%

Mitophagy reporter mouse analysis reveals increased mitophagy activity in disuse‐induced muscle atrophy

Yamashita

Kyuuma

Inoue

et al. 2021

Journal Cellular Physiology

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Muscle disuse induces atrophy through increased reactive oxygen species (ROS) released from damaged mitochondria. Mitophagy, the autophagic degradation of mitochondria, is associated with increased ROS production. However, the mitophagy activity status during disuse-induced muscle atrophy has been a subject of debate. Here, we developed a new mitophagy reporter mouse line to examine how disuse affected mitophagy activity in skeletal muscles. Mice expressing tandem mCherry-EGFP proteins on mitochondria were then used to monitor the dynamics of mitophagy activity. The reporter mice demonstrated enhanced mitophagy activity and increased ROS production in atrophic soleus muscles following a 14-day hindlimb immobilization. Results also showed an increased expression of multiple mitophagy genes, including Bnip3, Bnip3l, and Park2. Our findings thus conclude that disuse enhances mitophagy activity and ROS production in atrophic skeletal muscles and suggests that mitophagy is a potential therapeutic target for disuse-induced muscle atrophy.

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“…However, ROS are also related to disuse muscle atrophy [ 68 , 69 ]. Paradoxically, both skeletal muscle contraction and disuse or inactivity are associated with an increase in ROS generation leading to very different outcomes in the muscle cell [ 70 ]. An excessive ROS load is detrimental to muscle function and skeletal muscle sarcopenia, the decline in muscle mass and function commonly associated with ageing, is a phenotypic manifestation of underlying oxidative stress [ 71 , 72 ].…”

Section: Introductionmentioning

confidence: 99%

Redox-related biomarkers in physical exercise

et al. 2021

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Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake's group calculating the content of free radicals in skeletal muscle in resting conditions in 1954, many discoveries have been made in the field. The first section of this review is devoted to highlight the main research findings and fundamental changes in the exercise redox biology discipline. It includes: i) the first steps in free radical research, ii) the relation between exercise and oxidative damage, iii) the redox regulation of muscle fatigue, iv) the sources of free radicals during muscle contractions, and v) the role of reactive oxygen species as regulators of gene transcription and adaptations in skeletal muscle. In the second section of the manuscript, we review the available biomarkers for assessing health, performance, recovery during exercise training and overtraining in the sport population. Among the set of biomarkers that could be determined in exercise studies we deepen on the four categories of redox biomarkers: i) oxidants, ii) antioxidants, iii) oxidation products (markers of oxidative damage), and iv) measurements of the redox balance (markers of oxidative stress). The main drawbacks, strengths, weaknesses, and methodological considerations of every biomarker are also discussed.

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Redox modulation of muscle mass and function

Cited by 29 publications

References 192 publications

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Redox Signaling and Sarcopenia: Searching for the Primary Suspect

Mitophagy reporter mouse analysis reveals increased mitophagy activity in disuse‐induced muscle atrophy

Redox-related biomarkers in physical exercise

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