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Several marker proteins have the potential to increase their expression during the skeletal muscle atrophy process [17].
Thus, these findings from both human cancer patients and animal models of cancer cachexia strongly support the involvement of FoxO in driving the muscle atrophy process.
We hypothesize that the expression of the embryonic myosin heavy chain in the affected fibers is part of a compensatory response to the ongoing muscle atrophy process.
The decrease in Akt activity by PI-3k results in a higher activation of transcription factors, such as FOXOs, which might lead to a higher transcription of E3 ligases involved in the muscle atrophy process [ 14].
Many molecular pathways have been reported to be involved in the muscle atrophy process (Bodine et al., 2001b; Bodine et al., 2001a; Pallafacchina et al., 2002; Mammucari et al., 2007).
These hub nodes point to six different pathways that could be therefore considered as central for muscle atrophy process; these are the TGF-β pathway, apoptosis, membrane trafficking/cytoskeleton organization, NFKB pathway, inflammation and reorganization of the extracellular matrix.
Similar(54)
In order to elucidate whether the up-regulated MST1 kinase exerts any functional influence on neurogenic muscle atrophy, we examined atrophy process in muscles from three- to five-month-old adult WT and MST1 KO littermate mice.
The rapid increase in MST1 protein levels in fast-dominant muscles during denervation-induced atrophy suggests that MST1 kinase may functionally contribute to the muscle wasting process.
This study suggests that DEX-induced muscle atrophy is a dynamic process which involves important signaling factors over time.
Together, these findings revealed that muscle atrophy is an active process controlled by specific signaling pathways and transcriptional programs.
Significant advancements have been recently made in the understanding of the signalling pathways mediating skeletal muscle atrophy and its opposite process of hypertrophy [ 4- 9].
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