Myostatin (MSTN), also known as Growth Differentiation Factor-8 (GDF-8), is a member of the transforming growth factor-β superfamily. It is a negative regulator of skeletal muscle growth and development, inhibiting the proliferation of myoblasts. MSTN is crucial for maintaining the proper balance of muscle mass and is also involved in metabolism [2,4,5]. Genetic models, such as gene-edited animals, are valuable for studying its functions.

In livestock, MSTN-edited pigs (MSTN+/-) have higher muscle depth and lower fat depth without developmental problems, and there are no significant differences in the histomorphology of digestive and reproductive organs compared to wild-type pigs [1]. In goats, mutations of the MSTN gene induced by TALENs technology cause extensive skeletal muscle hyperplasia and hypertrophy, resulting in "double muscle" symptoms, reducing fat differentiation and increasing muscle content [2]. In sheep, a MSTNDel73C mutation with FGF5 knockout produced by Nuclease technology shows a dominant "double-muscle" phenotype, promoting skeletal muscle myofiber hyperplasia through the MEK-ERK-FOSL1 axis [3]. In Hu sheep, MSTN-edited using the C-CRISPR system have a double-muscled phenotype, with enhanced AKT and suppressed ERK1/2 signaling in the gluteus muscle [6].

In conclusion, MSTN is a key negative regulator of skeletal muscle growth and also plays a role in metabolism. Gene-edited animal models, especially those with MSTN mutations, have demonstrated its importance in enhancing muscle mass and potentially improving meat production in livestock. This research provides a foundation for understanding the biological functions of MSTN and its potential applications in animal breeding and muscle-related disease treatment.