Nearly 40–50% of total body mass in non-obese mammals is composed by skeletal muscles. In this review we outline the current knowledge linking mitochondria-dependent signaling pathways to muscle homeostasis in aging and disease and the resulting implications for the development of novel therapeutic approaches to prevent muscle loss. Optimized mitochondrial function is strictly maintained by the coordinated activation of different mitochondrial quality control pathways.
Exercise, on the other hand, improves mitochondrial function by activating mitochondrial biogenesis and mitophagy, possibly playing an important part in the beneficial effects of physical activity in several diseases. Moreover, dysfunctional mitochondria trigger catabolic signaling pathways which feed-forward to the nucleus to promote the activation of muscle atrophy. The changes of mitochondrial network influence the production of reactive oxygen species (ROS) that play an important role in muscle function. In these catabolic conditions the mitochondrial content, morphology and function are greatly affected. Loss of muscle mass and force occurs in many diseases such as disuse/inactivity, diabetes, cancer, renal, and cardiac failure and in aging-sarcopenia.
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