Abstract
Myostatin is an endogenous, negative regulator of muscle growth determining both muscle fiber number and size. The myostatin pathway is conserved across diverse species ranging from zebrafish to humans. Experimental models of muscle growth and regeneration have implicated myostatin as an important mediator of catabolic pathways in muscle cells. Inhibition of this pathway has emerged as a promising therapy for muscle wasting. Here we discuss the recent developments and the controversies in myostatin research, focusing on the molecular and cellular mechanisms underlying the actions of myostatin on skeletal muscle and the potential therapeutic role of myostatin on muscle-related disorders.
Highlights
Myostatin, known as GDF8, belongs to the transforming growth factor- superfamily of secreted growth and differentiation factors [1]
After cleavage of the signal sequence and proteolytic processing, the mature C-terminal dimer remains associated with the propeptide via non-covalent forces creating a latent complex from which myostatin must be released to elicit its biological activity [3,4,5,6]
Their results revealed that such decrease in specific force is associated with mitochondrial depletion and loss of oxydative characteristics of skeletal muscle. Based on these observations it appears that excessive muscle growth following deficiency in myostatin compromises force generation. These results suggest that muscle hypertrophy due to myostatin absence may not be beneficial to skeletal muscle
Summary
Known as GDF8 (growth differentiation factor 8), belongs to the transforming growth factor- superfamily of secreted growth and differentiation factors [1]. Through a number of yeast two-hybrid system experiments, four binding partners of myostatin (follistatin, hSGT, Titin cap and decorin) have been defined in muscle [7,8,9,10] whereas two follistatin related proteins FLRG and GASP have be found to be complexed with myostatin in serum [11, 12]. These proteins are able to negatively regulate myostatin activation, secretion or receptor binding.
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