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Skeletal muscle growth, primarily occurring via hypertrophy, is the physiological process of increasing muscle fiber size and total muscle mass in response to stimuli such as resistance exercise, hormonal signals, and nutritional intake [1, 11]. It is governed by a complex interplay between protein synthesis and degradation, where a net positive protein balance leads to mass accumulation [5]. Key regulatory pathways include the Mechanistic Target of Rapamycin (mTOR) signaling axis, which integrates nutrient and growth factor signals to drive protein synthesis, and the Myostatin/Smad pathway, which serves as a potent negative regulator of muscle size [9, 14]. While often discussed in the context of athletic performance, skeletal muscle growth is a critical therapeutic objective for treating wasting conditions such as sarcopenia, cancer-related cachexia, and muscular dystrophies [6, 13]. Drugs targeting this process typically modulate specific molecular components like the Androgen Receptor (AR), Myostatin (GDF-8), or the IGF-1 receptor rather than targeting 'growth' as a single entity [8, 12]. Consequently, 'Skeletal muscle growth' is characterized as a biological process rather than a discrete therapeutic target [2].
Drugs promoting this process typically function through Androgen Receptor agonism, Myostatin inhibition (e.g., via ActRIIB blockade), or activation of the IGF-1/mTOR signaling axis to stimulate protein synthesis and suppress protein breakdown [1, 5, 8, 14].
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