Figure 2.

Mitochondrial dysfunction arising from conditions of prolonged muscle inactivity, aging, chemotherapy, cancer, and sepsis, resulting in muscle wasting. Decreased respiratory capacity decreases ATP content and activates AMPK signaling. Increased ROS emissions activate the major proteolytic pathways and inactivates muscle protein synthesis pathways. The release of mitochondrial-derived proapoptotic factors activates caspase-3 and mediates myonuclear apoptosis.