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. Mutations in MSTN can lead to extensive skeletal muscle hyperplasia and hypertrophy, resulting in a "double-muscle" phenotype [1]. It is also involved in regulating energy homeostasis [5].

Mutations of the MSTN gene in various animals have been studied. In goats, TALENs technology was used to modify the MSTN gene, obtaining mutant cell lines and cloned goats with "double-muscle" phenotypes, which had increased muscle content [1]. In sheep, a MSTNDel73C mutation with FGF5 knockout via Nuclease technology led to a dominant "double-muscle" phenotype, promoting skeletal muscle myofiber hyperplasia [2]. In Hu sheep, the C-CRISPR system was used to generate MSTN-edited sheep with a double-muscled phenotype and enhanced AKT and suppressed ERK1/2 signaling in gluteus muscle [6]. In cattle, MSTN knockout cattle were produced via CRISPR-Cas9, and the MSTN mutation was transmitted from germ cells [4]. In athletes, the MSTN rs1805086 polymorphism was associated with the strength phenotype [3].

In conclusion, MSTN is a crucial negative regulator of skeletal muscle growth. Studies using gene-edited animal models have revealed its significant role in muscle development, energy homeostasis, and its potential association with athletic performance. These findings may have implications for livestock breeding, muscle-related disease treatment, and understanding human physical capabilities [1,2,3,4,5,6].