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10.1186/s13395-015-0033-y http://scihub22266oqcxt.onion/10.1186/s13395-015-0033-y C4381453!4381453!25834726     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Skelet+Muscle 2015 ; 5 (ä): ä Nephropedia Template TP {{tp|p=25834726|t=2015. PGC-1? modulates denervation-induced mitophagy in skeletal muscle |pdf=|usr=}}{{25834726}} gab.com Text PGC-1 modulates denervation-induced mitophagy in skeletal muscle JO: Skelet Muscle http://www.kidney.de/pget.php?&tw=1&pmid=25834726 #FOAvip Background: Alterations in skeletal muscle contractile activity necessitate an efficient remodeling mechanism. In particular, mitochondrial turnover is essential for tissue homeostasis during muscle adaptations to chronic use and disuse. While mitochondrial biogenesis appears to be largely governed by the transcriptional co-activator peroxisome proliferator co-activator 1 alpha (PGC-1?), selective mitochondrial autophagy (mitophagy) is thought to mediate organelle degradation. However, whether PGC-1? plays a direct role in autophagy is currently unclear. Methods: To investigate the role of the co-activator in autophagy and mitophagy during skeletal muscle remodeling, PGC-1? knockout (KO) and overexpressing (Tg) animals were unilaterally denervated, a common model of chronic muscle disuse. Results: Animals lacking PGC-1? exhibited diminished mitochondrial density alongside myopathic characteristics reminiscent of autophagy-deficient muscle. Denervation promoted an induction in autophagy and lysosomal protein expression in wild-type (WT) animals, which was partially attenuated in KO animals, resulting in reduced autophagy and mitophagy flux. PGC-1? overexpression led to an increase in lysosomal capacity as well as indicators of autophagy flux but exhibited reduced localization of LC3II and p62 to mitochondria, compared to WT animals. A correlation was observed between the levels of the autophagy-lysosome master regulator transcription factor EB (TFEB) and PGC-1? in muscle, supporting their coordinated regulation. Conclusions: Our investigation has uncovered a regulatory role for PGC-1? in mitochondrial turnover, not only through biogenesis but also via degradation using the autophagy-lysosome machinery. This implies a PGC-1?-mediated cross-talk between these two opposing processes, working to ensure mitochondrial homeostasis during muscle adaptation to chronic disuse. Electronic supplementary material: The online version of this article (doi:10.1186/s13395-015-0033-y) contains supplementary material, which is available to authorized users. Twit Text FOAVip PGC-1 modulates denervation-induced mitophagy in skeletal muscle ????Skelet Muscle http://www.kidney.de/pget.php?&tw=1&pmid=25834726 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25834726 #FOAvip English Wikipedia <ref>{{Cite pmid|25834726}}</ref> PGC-1? modulates denervation-induced mitophagy in skeletal muscle #MMPMID25834726 Vainshtein A; Desjardins EM; Armani A; Sandri M; Hood DA Skelet Muscle 2015[]; 5 (ä): ä PMID25834726show ga Background: Alterations in skeletal muscle contractile activity necessitate an efficient remodeling mechanism. In particular, mitochondrial turnover is essential for tissue homeostasis during muscle adaptations to chronic use and disuse. While mitochondrial biogenesis appears to be largely governed by the transcriptional co-activator peroxisome proliferator co-activator 1 alpha (PGC-1?), selective mitochondrial autophagy (mitophagy) is thought to mediate organelle degradation. However, whether PGC-1? plays a direct role in autophagy is currently unclear. Methods: To investigate the role of the co-activator in autophagy and mitophagy during skeletal muscle remodeling, PGC-1? knockout (KO) and overexpressing (Tg) animals were unilaterally denervated, a common model of chronic muscle disuse. Results: Animals lacking PGC-1? exhibited diminished mitochondrial density alongside myopathic characteristics reminiscent of autophagy-deficient muscle. Denervation promoted an induction in autophagy and lysosomal protein expression in wild-type (WT) animals, which was partially attenuated in KO animals, resulting in reduced autophagy and mitophagy flux. PGC-1? overexpression led to an increase in lysosomal capacity as well as indicators of autophagy flux but exhibited reduced localization of LC3II and p62 to mitochondria, compared to WT animals. A correlation was observed between the levels of the autophagy-lysosome master regulator transcription factor EB (TFEB) and PGC-1? in muscle, supporting their coordinated regulation. Conclusions: Our investigation has uncovered a regulatory role for PGC-1? in mitochondrial turnover, not only through biogenesis but also via degradation using the autophagy-lysosome machinery. This implies a PGC-1?-mediated cross-talk between these two opposing processes, working to ensure mitochondrial homeostasis during muscle adaptation to chronic disuse. Electronic supplementary material: The online version of this article (doi:10.1186/s13395-015-0033-y) contains supplementary material, which is available to authorized users. äPGC-1? modulates denervation-induced mitophagy in skeletal muscle (epmc).pdf DeepDyve Pubget Overpricing