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10.1152/ajpheart.00280.2014 http://scihub22266oqcxt.onion/10.1152/ajpheart.00280.2014 C4217009!4217009 !25172896     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25172896 &cmd=llinks): Failed to open stream: HTTP request failed! 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Promoting PGC-1?-driven mitochondrial biogenesis is detrimental in pressure-overloaded mouse hearts |pdf=|usr=}}{{25172896 }} gab.com Text Promoting PGC-1 -driven mitochondrial biogenesis is detrimental in pressure-overloaded mouse hearts JO: Am J Physiol Heart Circ Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25172896 #FOAvip Mitochondrial dysfunction in animal models of heart failure is associated with downregulation of the peroxisome proliferator-activated receptor-? coactivator (PGC)-1? pathway. To test whether PGC-1? is an appropriate therapeutic target for increasing mitochondrial biogenesis and improving function in heart failure, we used a transgenic (TG) mouse model of moderate overexpression of PGC-1? (?3-fold) in the heart. TG mice had small increases in citrate synthase activity and mitochondria size in the heart without alterations in myocardial energetics or cardiac function at baseline. In vivo dobutamine stress increased fractional shortening in wild-type mice, but this increase was attenuated in TG mice, whereas ex vivo isolated perfused TG hearts demonstrated normal functional and energetic response to high workload challenge. When subjected to pressure overload by transverse aortic constriction (TAC), TG mice displayed a significantly greater acute mortality for both male and female mice; however, long-term survival up to 8 wk was similar between the two groups. TG mice also showed a greater decrease in fractional shortening and a greater increase in left ventricular chamber dimension in response to TAC. Mitochondrial gene expression and citrate synthase activity were mildly increased in TG mice compared with wild-type mice, and this difference was also maintained after TAC. Our data suggest that a moderate level of PGC-1? overexpression in the heart compromises acute survival and does not improve cardiac function during chronic pressure overload in mice. Twit Text FOAVip Promoting PGC-1 -driven mitochondrial biogenesis is detrimental in pressure-overloaded mouse hearts ????Am J Physiol Heart Circ Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25172896 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25172896 #FOAvip English Wikipedia <ref>{{Cite pmid|25172896 }}</ref> Promoting PGC-1?-driven mitochondrial biogenesis is detrimental in pressure-overloaded mouse hearts #MMPMID25172896 Karamanlidis G ; Garcia-Menendez L ; Kolwicz SC Jr ; Lee CF ; Tian R Am J Physiol Heart Circ Physiol 2014[Nov]; 307 (9 ): H1307-16 PMID25172896 show ga Mitochondrial dysfunction in animal models of heart failure is associated with downregulation of the peroxisome proliferator-activated receptor-? coactivator (PGC)-1? pathway. To test whether PGC-1? is an appropriate therapeutic target for increasing mitochondrial biogenesis and improving function in heart failure, we used a transgenic (TG) mouse model of moderate overexpression of PGC-1? (?3-fold) in the heart. TG mice had small increases in citrate synthase activity and mitochondria size in the heart without alterations in myocardial energetics or cardiac function at baseline. In vivo dobutamine stress increased fractional shortening in wild-type mice, but this increase was attenuated in TG mice, whereas ex vivo isolated perfused TG hearts demonstrated normal functional and energetic response to high workload challenge. When subjected to pressure overload by transverse aortic constriction (TAC), TG mice displayed a significantly greater acute mortality for both male and female mice; however, long-term survival up to 8 wk was similar between the two groups. TG mice also showed a greater decrease in fractional shortening and a greater increase in left ventricular chamber dimension in response to TAC. Mitochondrial gene expression and citrate synthase activity were mildly increased in TG mice compared with wild-type mice, and this difference was also maintained after TAC. Our data suggest that a moderate level of PGC-1? overexpression in the heart compromises acute survival and does not improve cardiac function during chronic pressure overload in mice. |*Mitochondrial Turnover [MESH] |Animals [MESH] |Citrate (si)-Synthase/genetics/metabolism [MESH] |Female [MESH] |Heart Failure/*metabolism/physiopathology [MESH] |Male [MESH] |Mice [MESH] |Mitochondria, Heart/*metabolism/ultrastructure [MESH] |Myocardial Contraction [MESH] |Transcription Factors/genetics/*metabolism [MESH]Promoting PGC-1?-driven mitochondrial biogenesis is detrimental in p(epmc).pdf DeepDyve Pubget Overpricing