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10.4239/wjd.v6.i7.943 http://scihub22266oqcxt.onion/10.4239/wjd.v6.i7.943 C4499528!4499528!26185602     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       World+J+Diabetes 2015 ; 6 (7): 943-60 Nephropedia Template TP {{tp|p=26185602|t=2015. Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy |pdf=|usr=}}{{26185602}} gab.com Text Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy JO: World J Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=26185602 #FOAvip Diabetes mellitus significantly increases the risk of cardiovascular disease and heart failure in patients. Independent of hypertension and coronary artery disease, diabetes is associated with a specific cardiomyopathy, known as diabetic cardiomyopathy (DCM). Four decades of research in experimental animal models and advances in clinical imaging techniques suggest that DCM is a progressive disease, beginning early after the onset of type 1 and type 2 diabetes, ahead of left ventricular remodeling and overt diastolic dysfunction. Although the molecular pathogenesis of early DCM still remains largely unclear, activation of protein kinase C appears to be central in driving the oxidative stress dependent and independent pathways in the development of contractile dysfunction. Multiple subcellular alterations to the cardiomyocyte are now being highlighted as critical events in the early changes to the rate of force development, relaxation and stability under pathophysiological stresses. These changes include perturbed calcium handling, suppressed activity of aerobic energy producing enzymes, altered transcriptional and posttranslational modification of membrane and sarcomeric cytoskeletal proteins, reduced actin-myosin cross-bridge cycling and dynamics, and changed myofilament calcium sensitivity. In this review, we will present and discuss novel aspects of the molecular pathogenesis of early DCM, with a special focus on the sarcomeric contractile apparatus. Twit Text FOAVip Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy ????World J Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=26185602 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26185602 #FOAvip English Wikipedia <ref>{{Cite pmid|26185602}}</ref> Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy #MMPMID26185602 Waddingham MT; Edgley AJ; Tsuchimochi H; Kelly DJ; Shirai M; Pearson JT World J Diabetes 2015[Jul]; 6 (7): 943-60 PMID26185602show ga Diabetes mellitus significantly increases the risk of cardiovascular disease and heart failure in patients. Independent of hypertension and coronary artery disease, diabetes is associated with a specific cardiomyopathy, known as diabetic cardiomyopathy (DCM). Four decades of research in experimental animal models and advances in clinical imaging techniques suggest that DCM is a progressive disease, beginning early after the onset of type 1 and type 2 diabetes, ahead of left ventricular remodeling and overt diastolic dysfunction. Although the molecular pathogenesis of early DCM still remains largely unclear, activation of protein kinase C appears to be central in driving the oxidative stress dependent and independent pathways in the development of contractile dysfunction. Multiple subcellular alterations to the cardiomyocyte are now being highlighted as critical events in the early changes to the rate of force development, relaxation and stability under pathophysiological stresses. These changes include perturbed calcium handling, suppressed activity of aerobic energy producing enzymes, altered transcriptional and posttranslational modification of membrane and sarcomeric cytoskeletal proteins, reduced actin-myosin cross-bridge cycling and dynamics, and changed myofilament calcium sensitivity. In this review, we will present and discuss novel aspects of the molecular pathogenesis of early DCM, with a special focus on the sarcomeric contractile apparatus. äContractile apparatus dysfunction early in the pathophysiology of diab(epmc).pdf DeepDyve Pubget Overpricing