Research progress on molecular mechanism related to skeletal muscle atrophy.
- Author:
Yi-Bing KE
1
;
Dawuti ABUDOUKEREMU
1
;
Hao-Ran GUO
1
;
Yong-Ping WANG
2
Author Information
1. The 1st School of Clinical Medicine of Lanzhou University, Lanzhou 730000, China.
2. Department of Orthopaedics, the First Hospital of Lanzhou University, Lanzhou 730000, China.
- Publication Type:English Abstract
- MeSH:
Humans;
Muscular Atrophy/etiology*;
Muscle, Skeletal/pathology*;
Signal Transduction;
Animals;
Insulin-Like Growth Factor I/metabolism*;
Myostatin/physiology*;
TOR Serine-Threonine Kinases/metabolism*;
Autophagy/physiology*;
NF-kappa B/metabolism*;
Proteolysis;
Proteasome Endopeptidase Complex/physiology*
- From:
Acta Physiologica Sinica
2024;76(6):1056-1068
- CountryChina
- Language:Chinese
-
Abstract:
The maintenance of skeletal muscle quality involves various signal pathways that interact with each other. Under normal physiological conditions, these intersecting signal pathways regulate and coordinate the hypertrophy and atrophy of skeletal muscles, balancing the protein synthesis and degradation of muscle. When the total rate of protein synthesis exceeds that of protein degradation, the muscle gradually becomes enlarged, while when the total rate of protein synthesis is lower than that of protein degradation, the muscle shrinks. Myocyte atrophy mainly involves two protein degradation pathways, namely ubiquitin-proteasome and autophagy-lysosome. Protein degradation pathway is activated during muscle atrophy, resulting in the loss of muscle mass. Muscle atrophy can occur under various conditions such as malnutrition, aging and cachexia. Skeletal muscle atrophy caused by orthopedic diseases mainly includes disuse muscular atrophy caused by fracture and denervation muscular atrophy. The signal pathways that control and coordinate protein synthesis and degradation in skeletal muscle include insulin-like growth factor 1 (IGF1)-Akt-mammalian target of rapamycin (mTOR), myostatin-activin A-Smad, G protein α inhibitory peptide 2 (Gαi2)-PKC, nuclear factor κB (NF-κB), ectodysplasin A2 receptor (EDA2R)-NF-κB inducing kinase (NIK) and mitogen-activated protein kinase (MAPK) pathways. This paper provides a comprehensive review of the protein degradation pathways in skeletal muscle atrophy and the associated signal pathways regulating protein degradation in muscular atrophy.
