Postnatal inactivation of the myostatin gene in striated muscle caused generalized muscular hypertrophy of the same magnitude as that observed for constitutive myostatin knockout mice.
Does postnatal, muscle-specific inactivation of the myostatin gene cause muscular hypertrophy in mice?
Postnatal inactivation of myostatin in striated muscle causes generalized muscular hypertrophy, suggesting myostatin antagonists could be used to treat muscle wasting.
By using a conditional gene targeting approach exploiting the cre-lox system, we show that postnatal inactivation of the myostatin gene in striated muscle is sufficient to cause a generalized muscular hypertrophy of the same magnitude as that observed for constitutive myostatin knockout mice. This formally demonstrates that striated muscle is the production site of functional myostatin and that this member of the TGFbeta family of growth and differentiation factors regulates muscle mass not only during early embryogenesis but throughout development. It indicates that myostatin antagonist could be used to treat muscle wasting and to promote muscle growth in man and animals.
Grobet et al. (Thu,) conducted a other in Muscular hypertrophy. Postnatal inactivation of the myostatin gene in striated muscle vs. Constitutive myostatin knockout mice was evaluated on Generalized muscular hypertrophy. Postnatal inactivation of the myostatin gene in striated muscle caused generalized muscular hypertrophy of the same magnitude as that observed for constitutive myostatin knockout mice.
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