Muscle and oxidative stress

Ghiasvand, Reza; Hariri, Mitra

doi:10.1002/9781118832431.ch14

Oxidative Stress and Antioxidant Protection 2016

DOI: 10.1002/9781118832431.ch14

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Muscle and oxidative stress

Reza Ghiasvand

Mitra Hariri

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2023

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Taurine and Skeletal Muscle Disorders: Highlighting the Mitochondria-dependent Mechanisms

Heidari

Ommati

2023

Taurine and the Mitochondrion: Applications in the Pharmacotherapy of Human Diseases

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Skeletal muscle tissue contains a massive taurine (TAU) in millimolar concentrations. Several studies mentioned the importance of TAU in normal skeletal muscle function. It has been found that this amino acid plays a wide range of functions, ranging from osmoregulatory properties to the regulation of cytoplasmic Ca2+ homeostasis. Recent findings mentioned that TAU deficiency in the skeletal muscle leads to decreased exercise capacity, severe weakness, and muscle waste. On the other hand, it has been repeatedly shown that TAU supplementation could increase skeletal muscle performance in many disorders. These data mention the essential role of TAU in the skeletal muscle. Interestingly, it has been found that the effect of TAU on cellular mitochondria is an important feature of this amino acid in skeletal muscles. The current chapter highlights the physiological roles of TAU in muscle and its importance in the pathophysiology of skeletal muscle disorders. Then, the essential role of TAU in cellular mitochondria and its importance in muscle function is described. And the relevance of this amino acid in managing skeletal muscle pathologies is discussed.<br>

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Taurine and Skeletal Muscle Disorders: Highlighting the Mitochondria-dependent Mechanisms

Heidari

Ommati

2023

Taurine and the Mitochondrion: Applications in the Pharmacotherapy of Human Diseases

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show abstract

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Muscle and oxidative stress

Cited by 1 publication

References 77 publications

Taurine and Skeletal Muscle Disorders: Highlighting the Mitochondria-dependent Mechanisms

Taurine and Skeletal Muscle Disorders: Highlighting the Mitochondria-dependent Mechanisms

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