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10.1172/jci.insight.86898 http://scihub22266oqcxt.onion/10.1172/jci.insight.86898 C4882118!4882118!27239561     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27239561&cmd=llinks): Failed to open stream: HTTP request failed! 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Molecular profiling of dilated cardiomyopathy that progresses to heart failure |pdf=|usr=}}{{27239561}} gab.com Text Molecular profiling of dilated cardiomyopathy that progresses to heart failure JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=27239561 #FOAvip Dilated cardiomyopathy (DCM) is defined by progressive functional and structural changes. We performed RNA-seq at different stages of disease to define molecular signaling in the progression from pre-DCM hearts to DCM and overt heart failure (HF) using a genetic model of DCM (phospholamban missense mutation, PLNR9C/+). Pre-DCM hearts were phenotypically normal yet displayed proliferation of nonmyocytes (59% relative increase vs. WT, P = 8 × 10?4) and activation of proinflammatory signaling with notable cardiomyocyte-specific induction of a subset of profibrotic cytokines including TGF?2 and TGF?3. These changes progressed through DCM and HF, resulting in substantial fibrosis (17.6% of left ventricle [LV] vs. WT, P = 6 × 10?33). Cardiomyocytes displayed a marked shift in metabolic gene transcription: downregulation of aerobic respiration and subsequent upregulation of glucose utilization, changes coincident with attenuated expression of PPAR? and PPAR? coactivators -1? (PGC1?) and -1?, and increased expression of the metabolic regulator T-box transcription factor 15 (Tbx15). Comparing DCM transcriptional profiles with those in hypertrophic cardiomyopathy (HCM) revealed similar and distinct molecular mechanisms. Our data suggest that cardiomyocyte-specific cytokine expression, early fibroblast activation, and the shift in metabolic gene expression are hallmarks of cardiomyopathy progression. Notably, key components of these profibrotic and metabolic networks were disease specific and distinguish DCM from HCM. Twit Text FOAVip Molecular profiling of dilated cardiomyopathy that progresses to heart failure ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=27239561 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27239561 #FOAvip English Wikipedia <ref>{{Cite pmid|27239561}}</ref> Molecular profiling of dilated cardiomyopathy that progresses to heart failure #MMPMID27239561 Burke MA; Chang S; Wakimoto H; Gorham JM; Conner DA; Christodoulou DC; Parfenov MG; DePalma SR; Eminaga S; Konno T; Seidman JG; Seidman CE JCI Insight ä[]; 1 (6): ä PMID27239561show ga Dilated cardiomyopathy (DCM) is defined by progressive functional and structural changes. We performed RNA-seq at different stages of disease to define molecular signaling in the progression from pre-DCM hearts to DCM and overt heart failure (HF) using a genetic model of DCM (phospholamban missense mutation, PLNR9C/+). Pre-DCM hearts were phenotypically normal yet displayed proliferation of nonmyocytes (59% relative increase vs. WT, P = 8 × 10?4) and activation of proinflammatory signaling with notable cardiomyocyte-specific induction of a subset of profibrotic cytokines including TGF?2 and TGF?3. These changes progressed through DCM and HF, resulting in substantial fibrosis (17.6% of left ventricle [LV] vs. WT, P = 6 × 10?33). Cardiomyocytes displayed a marked shift in metabolic gene transcription: downregulation of aerobic respiration and subsequent upregulation of glucose utilization, changes coincident with attenuated expression of PPAR? and PPAR? coactivators -1? (PGC1?) and -1?, and increased expression of the metabolic regulator T-box transcription factor 15 (Tbx15). Comparing DCM transcriptional profiles with those in hypertrophic cardiomyopathy (HCM) revealed similar and distinct molecular mechanisms. Our data suggest that cardiomyocyte-specific cytokine expression, early fibroblast activation, and the shift in metabolic gene expression are hallmarks of cardiomyopathy progression. Notably, key components of these profibrotic and metabolic networks were disease specific and distinguish DCM from HCM. äMolecular profiling of dilated cardiomyopathy that progresses to heart(epmc).pdf DeepDyve Pubget Overpricing