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Mitochondrial Isolation from Skeletal Muscle
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[Signaling pathways controlling skeletal muscle mass].

Li-Fang Zheng1, Pei-Jie Chen1, Wei-Hua Xiao2

  • 1School of Kinesiology, Shanghai University of Sports, Shanghai 200438, China.

Sheng Li Xue Bao : [Acta Physiologica Sinica]
|August 24, 2019
PubMed
Summary

Maintaining skeletal muscle mass is vital for overall health. This review summarizes key signaling pathways controlling muscle growth and atrophy, influenced by exercise and disease.

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Area of Science:

  • Physiology
  • Molecular Biology
  • Biochemistry

Background:

  • Skeletal muscle constitutes over 40% of body weight and functions as a crucial endocrine organ.
  • Normal skeletal muscle mass is essential for physical activity and systemic organ function.
  • Factors like exercise and various diseases significantly impact skeletal muscle mass.

Purpose of the Study:

  • To review the critical signaling pathways involved in skeletal muscle mass regulation.
  • To highlight pathways promoting muscle hypertrophy and those driving muscle atrophy.
  • To provide an overview of how these pathways are modulated by physiological and pathological conditions.

Main Methods:

  • Literature review of signaling pathways in skeletal muscle mass control.
  • Analysis of molecular mechanisms underlying muscle hypertrophy and atrophy.
  • Synthesis of information on factors influencing these signaling pathways.

Main Results:

  • Resistance exercise promotes skeletal muscle hypertrophy via pathways like IGF-1/PI3K/Akt.
  • Muscle atrophy is associated with the activation of ubiquitin-proteasome, autophagy-lysosomal, NF-κB, and glucocorticoid pathways.
  • Specific signaling pathways, including myostatin and IGF-1/Akt/FoxO, are central to muscle mass regulation.

Conclusions:

  • Understanding these signaling pathways is crucial for maintaining skeletal muscle mass.
  • Dysregulation of these pathways contributes to muscle loss in various diseases.
  • Targeting these pathways may offer therapeutic strategies for muscle-related disorders.