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10.1161/CIRCRESAHA.116.306923 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.116.306923 C4888901!4888901!27230643     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       Circ+Res 2016 ; 118 (11): 1808-29 Nephropedia Template TP {{tp|p=27230643|t=2016. Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes |pdf=|usr=}}{{27230643}} gab.com Text Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=27230643 #FOAvip The clinical correlations linking diabetes with accelerated atherosclerosis, cardiomyopathy, and increased post-MI fatality rates are increasingly understood in mechanistic terms. The multiple mechanisms discussed in this review seem to share a common element: prolonged increases in ROS production in diabetic cardiovascular cells.Intracellular hyperglycemia causes excessive ROS production. This activates nuclear poly(ADP ribose) polymerase (PARP), which inhibits GAPDH, shunting early glycolytic intermediates into pathogenic signaling pathways. ROS and PARP also reduce sirtuin, PGC1?, and AMPK activity. These changes cause decreased mitochondrial biogenesis, increased ROS production, and disturbed circadian clock synchronization of glucose and lipid metabolism. Excessive ROS production also facilitates nuclear transport of pro-atherogenic transcription factors, increases transcription of the neutrophil enzyme initiating NETosis, PAD4, and activates the NRLP3 inflammasome.Insulin resistance causes excessive cardiomyocyte ROS production by increasing fatty acid flux and oxidation. This stimulates overexpression of the nuclear receptor PPAR? and nuclear translocation of FOXO1, which cause cardiomyopathy. ROS also shift the balance between mitochondrial fusion and fission in favor of increased fission, reducing the metabolic capacity and efficiency of the mitochondrial electron transport chain and ATP synthesis.Mitochondrial oxidative stress also plays a central role in angiotensin II-induced gap junction remodeling and arrhythmogenesis. ROS contribute to sudden death in diabetics after MI by increasing post-translational protein modifications which cause increased ryanodine receptor phosphorylation and downregulation of SERCA2a transcription. Increased ROS also depress autonomic ganglion synaptic transmission by oxidizing the nAch receptor ?3 subunit, potentially contributing to the increased risk of fatal cardiac arrhythmias associated with diabetic cardiac autonomic neuropathy. Twit Text FOAVip Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=27230643 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27230643 #FOAvip English Wikipedia <ref>{{Cite pmid|27230643}}</ref> Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes #MMPMID27230643 Shah MS; Brownlee M Circ Res 2016[May]; 118 (11): 1808-29 PMID27230643show ga The clinical correlations linking diabetes with accelerated atherosclerosis, cardiomyopathy, and increased post-MI fatality rates are increasingly understood in mechanistic terms. The multiple mechanisms discussed in this review seem to share a common element: prolonged increases in ROS production in diabetic cardiovascular cells.Intracellular hyperglycemia causes excessive ROS production. This activates nuclear poly(ADP ribose) polymerase (PARP), which inhibits GAPDH, shunting early glycolytic intermediates into pathogenic signaling pathways. ROS and PARP also reduce sirtuin, PGC1?, and AMPK activity. These changes cause decreased mitochondrial biogenesis, increased ROS production, and disturbed circadian clock synchronization of glucose and lipid metabolism. Excessive ROS production also facilitates nuclear transport of pro-atherogenic transcription factors, increases transcription of the neutrophil enzyme initiating NETosis, PAD4, and activates the NRLP3 inflammasome.Insulin resistance causes excessive cardiomyocyte ROS production by increasing fatty acid flux and oxidation. This stimulates overexpression of the nuclear receptor PPAR? and nuclear translocation of FOXO1, which cause cardiomyopathy. ROS also shift the balance between mitochondrial fusion and fission in favor of increased fission, reducing the metabolic capacity and efficiency of the mitochondrial electron transport chain and ATP synthesis.Mitochondrial oxidative stress also plays a central role in angiotensin II-induced gap junction remodeling and arrhythmogenesis. ROS contribute to sudden death in diabetics after MI by increasing post-translational protein modifications which cause increased ryanodine receptor phosphorylation and downregulation of SERCA2a transcription. Increased ROS also depress autonomic ganglion synaptic transmission by oxidizing the nAch receptor ?3 subunit, potentially contributing to the increased risk of fatal cardiac arrhythmias associated with diabetic cardiac autonomic neuropathy. äMolecular and Cellular Mechanisms of Cardiovascular Disorders in Diabe(epmc).pdf DeepDyve Pubget Overpricing