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At this point, we have previously shown that IGF-I is a main character in restoring mitochondrial dysfunction during aging by increasing mitochondrial membrane potential, reducing oxygen consumption, and increasing ATP synthesis what in turn minimize the c-cytochrome release to the cytoplasm and subsequently promote neural survival by decreasing caspase-induced apoptosis [55,56], in agreement with in vitro reported works from others [242-244]

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They each have interplay with inflammation and although the most is known about NO, that does not mean it is the most important, only that it has been the most extensively investigated

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