The Journal of Physiology © 2014 The Physiological Society. Our results indicate that mitochondrial dysfunction plays a major role in disuse atrophy and that compounds inducing PGC-1α expression could be useful to treat/prevent muscle atrophy. Transgenic PGC-1α animals did not show metabolic alteration during unloading, preserving muscle size through the reduction of autophagy and proteasome degradation. To define the link between mitochondrial dysfunction and disuse muscle atrophy we unloaded mice overexpressing PGC-1α. PGC-1α and mitochondrial complexes were down-regulated and DRP1 was up-regulated. HU mice showed a marked alteration of oxidative metabolism. Trolox completely prevented the induction of NRF2, SOD1 and catalase mRNAs, but not atrophy or induction of catabolic systems in unloaded muscles, suggesting that oxidative stress is not a major cause of disuse atrophy. Uniprot Gene hsa:1 P04217 A1BG hsa:10 A4Z6T7 NAT2 hsa:10 P11245 NAT2 AAC2 hsa:100 A0A0S2Z381 ADA hCG38105 hsa:100 P00813 ADA ADA1 hsa:1000 A0A024RC42 CDH2 hCG22518 hsa:1000 P19022 CDH2 CDHN NCAD hsa:10000 Q9Y243 AKT3 PKBG hsa:100008586 O76087 GAGE7 GAGE12I GAGE7B hsa:100008586 P0CL80 GAGE12F hsa:100008586 P0CL81 GAGE12G hsa:100008586 P0CL82 GAGE12I hsa:10001 O75586 MED6 ARC33 hsa:10002. Lzip is a lossless data compressor with a user interface similar to the one of gzip or bzip2. As clzip is written in C, it may be easier to integrate in applications like package managers, embedded devices, or systems lacking a C++ compiler. PGC-1a protects against neurodegenerative diseases. Clzip is a C language version of lzip, fully compatible with lzip 1.4 or newer. This protein may be also involved in controlling blood pressure, regulating cellular cholesterol homeostasis, and the development of obesity. PGC-1 increases energy metabolism and weight loss. HU caused a reduction in cross-sectional area, redox status alteration (NRF2, SOD1 and catalase up-regulation), and induction of the ubiquitin proteasome system (MuRF-1 and atrogin-1 mRNA up-regulation) and autophagy (Beclin1 and p62 mRNA up-regulation). PGC-1 makes new mitochondria and improves its function. First we studied the adaptations of soleus to mice hindlimb unloading (HU) in the early phase of disuse (3 and 7 days of HU) with and without antioxidant treatment (trolox). Here we hypothesized that a metabolic stress mediated by PGC-1α down-regulation plays a major role in disuse atrophy. PGC-1 helps to regulate cell processes important in adaptive thermogenesis and energy metabolism, including the related. Redox imbalance has been considered one of the major triggers of skeletal muscle disuse atrophy, but whether redox imbalance is actually the major cause or simply a consequence of muscle disuse remains of debate. Named for its association with the nuclear receptor peroxisome-proliferator activated receptor (PPAR), PGC-1 interacts with a diverse array of transcription factors to regulate numerous aspects of cell physiology (2). Prolonged skeletal muscle inactivity causes muscle fibre atrophy.
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