Acts specifically as a negative regulator of skeletal muscle growth. Homodimer; disulfide-linked. Interacts with WFIKKN2, leading to inhibit its activity. Interacts with FSTL3. Specifically expressed in developing and adult skeletal muscle. Highest levels found in the hindlimb semimembranosus and biceps-femoris muscles; low levels in other hindlimb muscles. Widely expressed throughout development. Low levels are found up to day 29 embryos. Levels increase from day 31 up until late gestation. Synthesized as large precursor molecule that undergoes proteolytic cleavage to generate an N-terminal propeptide and a disulfide linked C-terminal dimer, which is the biologically active molecule. The circulating form consists of a latent complex of the C-terminal dimer and other proteins, including its propeptide, which maintain the C-terminal dimer in a latent, inactive state. Ligand activation requires additional cleavage of the prodomain by a tolloid-like metalloproteinase. Defects in MSTN are the cause of the double-muscle phenotype or muscular hypertrophy (mh), an autosomal recessive disease frequently found in the Belgian blue and Piedmontese cattle breeds. This disease is characterized by an increased number of muscle fibers (hyperplasia), resulting in an increase in muscle mass of 20-25%. Belongs to the TGF-beta family.