Assessing the Function and Control of miR-322(424)/503 on Skeletal Muscle
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Muscle atrophy, a common complication of many diseases such as cancer, COPD, and heart failure, has no effective treatment approaches to date. Recently, we identified miR-322/503 as a significant regulator of muscle homeostasis and may play an important role in muscular degenerative diseases. Our objective is to explore the phenotypes and mechanisms of skeletal muscle-specific overexpression and the knock-out of miR-322/503. We found that miR-322/503 regulated skeletal muscle homeostasis through inhibition of elF4E and elF4G1, which are two critical components in translation initiation process.