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10.15252/emmm.201404669 http://scihub22266oqcxt.onion/10.15252/emmm.201404669 C4568954!4568954!26160456     free     free     free Deprecated: Implicit conversion from float 223.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 223.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 223.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 223.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 223.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 223.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 257.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 257.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 257.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2015 ; 7 (9): 1229-43 Nephropedia Template TP {{tp|p=26160456|t=2015. Cardiac LXR? protects against pathological cardiac hypertrophy and dysfunction by enhancing glucose uptake and utilization |pdf=|usr=}}{{26160456}} gab.com Text Cardiac LXR protects against pathological cardiac hypertrophy and dysfunction by enhancing glucose uptake and utilization JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26160456 #FOAvip Pathological cardiac hypertrophy is characterized by a shift in metabolic substrate utilization from fatty acids to glucose, but the molecular events underlying the metabolic remodeling remain poorly understood. Here, we investigated the role of liver X receptors (LXRs), which are key regulators of glucose and lipid metabolism, in cardiac hypertrophic pathogenesis. Using a transgenic approach in mice, we show that overexpression of LXR? acts to protect the heart against hypertrophy, fibrosis, and dysfunction. Gene expression profiling studies revealed that genes regulating metabolic pathways were differentially expressed in hearts with elevated LXR?. Functionally, LXR? overexpression in isolated cardiomyocytes and murine hearts markedly enhanced the capacity for myocardial glucose uptake following hypertrophic stress. Conversely, this adaptive response was diminished in LXR?-deficient mice. Transcriptional changes induced by LXR? overexpression promoted energy-independent utilization of glucose via the hexosamine biosynthesis pathway, resulting in O-GlcNAc modification of GATA4 and Mef2c and the induction of cytoprotective natriuretic peptide expression. Our results identify LXR? as a key cardiac transcriptional regulator that helps orchestrate an adaptive metabolic response to chronic cardiac stress, and suggest that modulating LXR? may provide a unique opportunity for intervening in myocyte metabolism. Twit Text FOAVip Cardiac LXR protects against pathological cardiac hypertrophy and dysfunction by enhancing glucose uptake and utilization ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26160456 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26160456 #FOAvip English Wikipedia <ref>{{Cite pmid|26160456}}</ref> Cardiac LXR? protects against pathological cardiac hypertrophy and dysfunction by enhancing glucose uptake and utilization #MMPMID26160456 Cannon MV; Silljé HH; Sijbesma JW; Vreeswijk-Baudoin I; Ciapaite J; van der Sluis B; van Deursen J; Silva GJ; de Windt LJ; Gustafsson JÅ; van der Harst P; van Gilst WH; de Boer RA EMBO Mol Med 2015[Sep]; 7 (9): 1229-43 PMID26160456show ga Pathological cardiac hypertrophy is characterized by a shift in metabolic substrate utilization from fatty acids to glucose, but the molecular events underlying the metabolic remodeling remain poorly understood. Here, we investigated the role of liver X receptors (LXRs), which are key regulators of glucose and lipid metabolism, in cardiac hypertrophic pathogenesis. Using a transgenic approach in mice, we show that overexpression of LXR? acts to protect the heart against hypertrophy, fibrosis, and dysfunction. Gene expression profiling studies revealed that genes regulating metabolic pathways were differentially expressed in hearts with elevated LXR?. Functionally, LXR? overexpression in isolated cardiomyocytes and murine hearts markedly enhanced the capacity for myocardial glucose uptake following hypertrophic stress. Conversely, this adaptive response was diminished in LXR?-deficient mice. Transcriptional changes induced by LXR? overexpression promoted energy-independent utilization of glucose via the hexosamine biosynthesis pathway, resulting in O-GlcNAc modification of GATA4 and Mef2c and the induction of cytoprotective natriuretic peptide expression. Our results identify LXR? as a key cardiac transcriptional regulator that helps orchestrate an adaptive metabolic response to chronic cardiac stress, and suggest that modulating LXR? may provide a unique opportunity for intervening in myocyte metabolism. äCardiac LXR? protects against pathological cardiac hypertrophy and dys(epmc).pdf DeepDyve Pubget Overpricing