Myostatin (MSTN), also known as GDF-8, is a protein belonging to the transforming growth factor-β superfamily. It serves as a negative regulator of skeletal muscle growth and development, inhibiting the activation and proliferation of muscle satellite cells and myoblasts [1,3,4]. The MSTN regulatory network involves genes related to muscle function, cell-cycle regulation, and signaling pathways such as Notch, MAPK, and WNT [3]. Mutations in MSTN are of great commercial value as they can improve livestock meat production [2].

In various animal models, MSTN inactivation has shown significant effects. In MSTN-edited heterozygous pigs, there were no significant differences in the histomorphology of digestive and reproductive organs compared to wild-type pigs, though the MSTN +/- pigs had higher muscle depth and lower fat depth [1]. In sheep, a MSTNDel73C mutation with FGF5 knockout led to a dominant 'double-muscle' phenotype, increased muscle fiber number, and smaller myotubes through the activation of the MEK-ERK-FOSL1 axis [2]. In goats, MSTN gene mutations obtained by TALENs technology resulted in tightly arranged and thick muscle fibers and higher monthly body weight in cloned goats [4]. In cattle, MSTN knockout (- 12bps deletion) could be germline-transmitted to the next generation without health issues [5]. In Hu sheep, MSTN-edited animals using C-CRISPR showed a double-muscled phenotype with higher body weight at 3 and 4 months old [6].

In conclusion, MSTN is a key negative regulator of skeletal muscle growth. Studies using gene-edited animal models, such as KO models in pigs, sheep, goats, cattle, and Hu sheep, have revealed its role in muscle development and the potential for improving livestock production. These findings provide valuable insights into the biological function of MSTN and its potential applications in animal breeding and muscle-related disease treatment.