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Myostatin (also known as growth differentiation factor 8, abbreviated GDF8) is a protein that in humans is encoded by the MSTN gene. [6] Myostatin is a myokine that is produced and released by myocytes and acts on muscle cells to inhibit muscle growth. [7] Myostatin is a secreted growth differentiation factor that is a member of the TGF beta ...
Myostatin-related muscle hypertrophy is a rare genetic condition characterized by reduced body fat and increased skeletal muscle size. [1] Affected individuals have up to twice the usual amount of muscle mass in their bodies, but increases in muscle strength are not usually congruent. [ 2 ]
Myostatin inhibitors are a class of drugs that work by blocking the effect of myostatin, which inhibits muscle growth. In animal models and limited human studies, myostatin inhibitors have increased muscle size. They are being developed to treat obesity, sarcopenia, muscular dystrophy, and other illnesses.
Double-muscled cattle are breeds of cattle that carry one of seven known mutations that limits and reduces the activity of the myostatin protein. Normally, myostatin limits the number of muscle fibers present at birth, and interfering with activity of this protein causes animals to be born with higher numbers of muscle fibers, consequently augmenting muscle growth.
The definition and use of the term myokine first occurred in 2003. [5] In 2008, the first myokine, myostatin, was identified. [4] [6] The gp130 receptor cytokine IL-6 (Interleukin 6) was the first myokine found to be secreted into the blood stream in response to muscle contractions.
Myostatin, a TGF-beta superfamily member, is a negative regulator of muscle growth. [1] Myostatin binds to ACVR2B and to a lesser extent ACVR2A. In mice that were ACVR2A −/− mutants there was an increase in all four muscle groups studied (pectoralis, triceps, quadriceps, and gastrocnemious/plantaris muscles). [1] Two of these muscle groups ...
As muscle hypertrophy is a response to strenuous anaerobic activity, ordinary everyday activity would become strenuous in diseases that result in premature muscle fatigue (neural or metabolic), or disrupt the excitation-contraction coupling in muscle, or cause repetitive or sustained involuntary muscle contractions (fasciculations, myotonia, or ...
The exact cause is unclear. A combination of consistent findings on physical examination, the presence of anti HMG-CoA reductase antibodies in a person with myopathy, evidence of muscle breakdown, and muscle biopsy diagnose SAAM. [3] Treatment involves stopping the associated statin medication and taking medication to suppress the immune system.