4.7 Review

Mitochondrial Function and Reactive Oxygen/Nitrogen Species in Skeletal Muscle

Journal

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2022.826981

Keywords

skeletal muscle; mitochondrial function; mitochondrial dynamics; RONS; oxidative stress

Funding

  1. Natural Science Foundation of China [32072722]
  2. National Transgenic Creature Breeding Grand Project [2016zx08008-003]

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Mitochondria in skeletal muscle play an important role in producing ATP for muscle contraction, but also produce reactive species as byproducts. Traditionally, an increase in reactive oxygen/nitrogen species (RONS) is associated with oxidative stress and muscle dysfunction, but recent studies have highlighted the physiological significance of an optimal RONS level in skeletal muscle under the influence of antioxidants.
Skeletal muscle fibers contain a large number of mitochondria, which produce ATP through oxidative phosphorylation (OXPHOS) and provide energy for muscle contraction. In this process, mitochondria also produce several types of reactive species as side product, such as reactive oxygen species and reactive nitrogen species which have attracted interest. Mitochondria have been proven to have an essential role in the production of skeletal muscle reactive oxygen/nitrogen species (RONS). Traditionally, the elevation in RONS production is related to oxidative stress, leading to impaired skeletal muscle contractility and muscle atrophy. However, recent studies have shown that the optimal RONS level under the action of antioxidants is a critical physiological signal in skeletal muscle. Here, we will review the origin and physiological functions of RONS, mitochondrial structure and function, mitochondrial dynamics, and the coupling between RONS and mitochondrial oxidative stress. The crosstalk mechanism between mitochondrial function and RONS in skeletal muscle and its regulation of muscle stem cell fate and myogenesis will also be discussed. In all, this review aims to describe a comprehensive and systematic network for the interaction between skeletal muscle mitochondrial function and RONS.

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