MSTN

Official Full Name

myostatin

Organism

Homo sapiens

GeneID

2660

Background

This gene encodes a secreted ligand of the TGF-beta (transforming growth factor-beta) superfamily of proteins. Ligands of this family bind various TGF-beta receptors leading to recruitment and activation of SMAD family transcription factors that regulate gene expression. The encoded preproprotein is proteolytically processed to generate each subunit of the disulfide-linked homodimer. This protein negatively regulates skeletal muscle cell proliferation and differentiation. Mutations in this gene are associated with increased skeletal muscle mass in humans and other mammals. [provided by RefSeq, Jul 2016]

Synonyms

GDF8; MSLHP;

Protein Sequence

MQKLQLCVYIYLFMLIVAGPVDLNENSEQKENVEKEGLCNACTWRQNTKSSRIEAIKIQILSKLRLETAPNISKDVIRQLLPKAPPLRELIDQYDVQRDDSSDGSLEDDDYHATTETIITMPTESDFLMQVDGKPKCCFFKFSSKIQYNKVVKAQLWIYLRPVETPTTVFVQILRLIKPMKDGTRYTGIRSLKLDMNPGTGIWQSIDVKTVLQNWLKQPESNLGIEIKALDENGHDLAVTFPGPGEDGLNPFLEVKVTDTPKRSRRDFGLDCDEHSTESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGECEFVFLQKYPHTHLVHQANPRGSAGPCCTPTKMSPINMLYFNGKEQIIYGKIPAMVVDRCGCS

Open

Disease

Idiopathic inflammatory myopathy, Muscular atrophy, Muscular dystrophy, Retinopathy

Approved Drug

Clinical Trial Drug

9 +

Discontinued Drug

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Detailed Information

Myostatin (MSTN), also known as myostatin, was a sequence of cDNA that was discovered by American scientist McPherron et al. in 1997 when studying transforming growth factor β (TGF-β) family members. After intensive research, the adult mice lacking the gene weighed about 25%-30% more than the wild type, and the mass of the monolayer muscles increased significantly compared with the wild mice, indicating that MSTN is a negative regulator of skeletal muscle growth.

Figure 1. Summary of myostatin function during muscle wasting and insulin resistance. (Sharma, M., et al. 2015)

Effect of MSTN on Muscle Tissue

MSTN can significantly inhibit muscle growth. The effect of MSTN on muscle is mainly reflected in the inhibition of prenatal muscle development and postpartum muscle hypertrophy. Studies have shown that the regulation of MSTN on muscle fibers is mainly reflected in two aspects: (1) regulating the number of muscle fibers during growth and development; and (2) regulating the growth and growth of muscle fibers after birth. The study found that MSTN overexpressing transgenic mice showed a significant decrease in muscle mass and muscle fiber area. MSTN knockout mice gained 30% of their body weight and 262% of wild-type mice. The regulation of muscle weight by MSTN is mainly achieved by down-regulating protein synthesis. Studies have shown that MSTN can inhibit the synthesis of myoblasts and some myotube proteins. The researchers examined the synthesis rate of myofibrillin in normal mice and MSTN-deficient mice and found that MSTN-deficient mice increased myofibrillin synthesis.

The Effect of Exercise on MSTN

Exercise can affect the expression of MSTN. In general, exercise can make bones hypertrophy, and MSTN is a negative regulator of skeletal muscle growth. It can be speculated that exercise may reduce the expression of MSTN. Experiments have shown that both repeated exercise and rapid and sustained exercise can reduce the expression of MSTN mRNA. Recent studies have found that in purebred horse racing, the genotype of MSTN is related to speed. In MSTN knockout mice, exercise can weaken the hypertrophic phenotype of the muscle and restore skeletal muscle function. Moderate-intensity endurance and strength exercises improve muscle function but have no significant effect on MSTN mRNA levels. Strength exercise with blood flow restriction can reduce the gene expression of MSTN. Studies have reported changes in muscle MSTN mRNA expression after acute exercise.

The effects of exercise on MSTN expression are also different due to different movement patterns, different parts of exercise, length of exercise, and persistence. In addition, the effect of exercise on MSTN expression is also affected by age, gender, and so on. Studies of young and old people showed that young people's MSTN mRNA levels were reduced by 50% after exercise, while older people did not. Recent studies have found that age-induced decrease in muscle mass and strength is associated with increased mRNA and protein expression of the gastrocnemius muscle MSTN. Further research is needed on the mechanism by which exercise affects MSTN and the quality of muscle mass. In addition, exercise can reduce the mRNA level of MSTN in muscle, but has no effect on the expression of MSTN in tendon.

References:

Sharma, M. , Mcfarlane, C. , Kambadur, R. , Kukreti, H. , Bonala, S. , & Srinivasan, S. . (2015). Myostatin: expanding horizons. IUBMB Life, 67(8), 589-600.
Assyov, Y. S. , Velikova, T. V. , & Kamenov, Z. A. . (2016). Myostatin and carbohydrate disturbances. Endocrine Research, 1-8.
Mariot, V. , Joubert, R. , Hourdé, Christophe, Féasson, Léonard, Hanna, M. , & Muntoni, F. , et al. (2017). Downregulation of myostatin pathway in neuromuscular diseases may explain challenges of anti-myostatin therapeutic approaches. Nature Communications, 8(1), 1859.

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