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In conclusion, our current data provide an explanation for previous observations indicating that cytoplasmic levels of Id2 and nuclear apoptosis are increased under conditions of muscle wasting including sarcopenia [26], [27].
Because muscle wasting is a cardinal feature of KD/SBMA and wasting is present in all 3 models, we were not surprised to find Fbxo32 in all of the gene lists (Table S4 and Table 1) However, Fbxo32 was unexpectedly decreased in all 3 models, whereas increases in Fbxo32 were observed in other cases of muscle wasting, including diabetes, renal failure, cancer and denervation [15], [30].
This is of clinical relevance since muscle wasting including accelerated protein breakdown and hyperglycemia are metabolic responses frequently observed in critically ill or severely injured patients.
Myostatin has been implicated in several forms of muscle wasting, including the severe cachexia observed as a result of conditions such as AIDS and liver cirrhosis.
By contrast, different pathologic conditions promoting muscle wasting, including cancer, are associated with elevated systemic levels of IL-6 [ 4].
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