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10.1161/CIRCULATIONAHA.116.022495 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.116.022495 C5193133!5193133!27489254     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circulation 2016 ; 134 (12): 883-94 Nephropedia Template TP {{tp|p=27489254|t=2016. Normalization of NAD+ Redox Balance as a Therapy for Heart Failure |pdf=|usr=}}{{27489254}} gab.com Text Normalization of NAD+ Redox Balance as a Therapy for Heart Failure JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=27489254 #FOAvip Background: heart failure has become increasingly prevalent along with the aging population and the increased survival of acute ischemic heart events. Impairments of mitochondrial function in the heart are intricately linked to the development of heart failure but there is no therapy for mitochondrial dysfunction in the clinic. Methods and Results: we report that NAD+ redox imbalance (increased NADH/NAD+) and protein hyperacetylation, previously observed in genetic models of defective mitochondrial function, are also present in human failing hearts as well as in mouse hearts with pathological hypertrophy. Elevation of NAD+ levels by stimulating the NAD+ salvage pathway suppressed mitochondrial protein hyperacetylation and cardiac hypertrophy, and improved cardiac function in responses to stresses. Acetylome analysis identified a subpopulation of mitochondrial proteins that was sensitive to changes in the NADH/NAD+ ratio. Hyperacetylation of mitochondrial malate-aspartate shuttle proteins impaired the transport and oxidation of cytosolic NADH in the mitochondria, resulting in altered cytosolic redox state and energy deficiency. Furthermore, acetylation of oligomycin-sensitive conferring protein at lysine-70 in ATP synthase complex promoted its interaction with cyclophilin D, and sensitized the opening of mitochondrial permeability transition pore. Both could be alleviated by normalizing the NAD+ redox balance either genetically or pharmacologically. Conclusions: we show that mitochondrial protein hyperacetylation due to NAD+ redox imbalance contributes to the pathological remodeling of the heart via two distinct mechanisms. Our preclinical data demonstrate a clear benefit of normalizing NADH/NAD+ imbalance in the failing hearts. These findings have a high translational potential as the pharmacological strategy of increasing NAD+ precursors are feasible in human. Twit Text FOAVip Normalization of NAD+ Redox Balance as a Therapy for Heart Failure ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=27489254 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27489254 #FOAvip English Wikipedia <ref>{{Cite pmid|27489254}}</ref> Normalization of NAD+ Redox Balance as a Therapy for Heart Failure #MMPMID27489254 Lee CF; Chavez JD; Garcia-Menendez L; Choi Y; Roe ND; Chiao YA; Edgar JS; Goo YA; Goodlett DR; Bruce JE; Tian R Circulation 2016[Sep]; 134 (12): 883-94 PMID27489254show ga Background: heart failure has become increasingly prevalent along with the aging population and the increased survival of acute ischemic heart events. Impairments of mitochondrial function in the heart are intricately linked to the development of heart failure but there is no therapy for mitochondrial dysfunction in the clinic. Methods and Results: we report that NAD+ redox imbalance (increased NADH/NAD+) and protein hyperacetylation, previously observed in genetic models of defective mitochondrial function, are also present in human failing hearts as well as in mouse hearts with pathological hypertrophy. Elevation of NAD+ levels by stimulating the NAD+ salvage pathway suppressed mitochondrial protein hyperacetylation and cardiac hypertrophy, and improved cardiac function in responses to stresses. Acetylome analysis identified a subpopulation of mitochondrial proteins that was sensitive to changes in the NADH/NAD+ ratio. Hyperacetylation of mitochondrial malate-aspartate shuttle proteins impaired the transport and oxidation of cytosolic NADH in the mitochondria, resulting in altered cytosolic redox state and energy deficiency. Furthermore, acetylation of oligomycin-sensitive conferring protein at lysine-70 in ATP synthase complex promoted its interaction with cyclophilin D, and sensitized the opening of mitochondrial permeability transition pore. Both could be alleviated by normalizing the NAD+ redox balance either genetically or pharmacologically. Conclusions: we show that mitochondrial protein hyperacetylation due to NAD+ redox imbalance contributes to the pathological remodeling of the heart via two distinct mechanisms. Our preclinical data demonstrate a clear benefit of normalizing NADH/NAD+ imbalance in the failing hearts. These findings have a high translational potential as the pharmacological strategy of increasing NAD+ precursors are feasible in human. äNormalization of NAD+ Redox Balance as a Therapy for Heart Failure (epmc).pdf DeepDyve Pubget Overpricing