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Mitochondrial-regulated apoptosis provides a strong signaling network that contributes to sarcopenia (8). We have taken the perspective that both neural and muscle components contribute to muscle wasting, but mitochondrial health is central to initiating and perpetuating the signal for sarcopenia. We argue that mitochondrial dysfunction leads to increased mPTP opening and initiates apoptotic signaling in muscle cells and motor neurons. In aging, this is not corrected because mitophagy is inhibited. Proteasome activation leads to removal of cellular contents close to the site of dysfunctional mitochondria, and this cellular dismantling expands proportionally to the accumulation of dysfunctional mitochondria. Although aging induces widespread systemic mitochondrial dysfunction, perhaps as a result of high ROS or accumulation of mtDNA damage, we have considered that retrograde and anterograde communication likely exists between dying muscle and motor neurons, which may accelerate death in both compartments. Additional studies are needed to establish if exercise and nutrition can be used to effectively improve mitochondria health and reduce sarcopenia in aging populations. In our view, targeting dysfunctional mitochondria and increasing healthy mitochondria in motor neurons and muscle fibers provide the best strategy for reducing sarcopenia.

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