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Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice.
It is shown that Sirt3 protects the mouse heart by blocking the cardiac hypertrophic response and is an endogenous negative regulator of cardiac hypertrophy, which protects hearts by suppressing cellular levels of ROS.
SIRT3 Is a Stress-Responsive Deacetylase in Cardiomyocytes That Protects Cells from Stress-Mediated Cell Death by Deacetylation of Ku70
It is found that SIRT3 is a stress-responsive deacetylase and that its increased expression protects myocytes from genotoxic and oxidative stress-mediated cell death, and identifies Ku70 as a new target of Sirt3.
Exogenous NAD Blocks Cardiac Hypertrophic Response via Activation of the SIRT3-LKB1-AMP-activated Kinase Pathway*
The results reveal a novel role of NAD as an inhibitor of cardiac hypertrophic signaling, and suggest that prevention of NAD depletion may be critical in the treatment of cardiac hypertrophy and heart failure.
SIRT3 Deacetylates and Activates OPA1 To Regulate Mitochondrial Dynamics during Stress
It is reported that OPA1, a mitochondrial fusion protein, was hyperacetylated in hearts under pathological stress and this posttranslational modification reduced the GTPase activity of the protein.
Poly(ADP-ribose) Polymerase-1-dependent Cardiac Myocyte Cell Death during Heart Failure Is Mediated by NAD+ Depletion and Reduced Sir2α Deacetylase Activity*
Depletion of cellular NAD levels forms a link between PARP activation and reduced Sir2α deacetylase activity, contributing to myocyte cell death during heart failure in stressed cardiac myocytes.
The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun
It is shown that sirtuin 6 (SIRT6), a nuclear histone deacetylase, functions at the level of chromatin to directly attenuate IGF-Akt signaling and implicate SIRT6 in the development of cardiac hypertrophy and failure.
The Deacetylase SIRT1 Promotes Membrane Localization and Activation of Akt and PDK1 During Tumorigenesis and Cardiac Hypertrophy
Deacetylation of Akt and its activating kinase PDK1 promotes cell growth in physiological and pathological settings. Deacetylation for Activation Cell growth can be physiological (such as when heart
Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial SIRT3
The results suggest that HKL is a pharmacological activator of SIRT3 capable of blocking, and even reversing, the cardiac hypertrophic response.
Obesity-induced lysine acetylation increases cardiac fatty acid oxidation and impairs insulin signalling.
Increased cardiac fatty acid oxidation in response to high-fat feeding is controlled, in part, via the down-regulation of SIRT3 and concomitant increased acetylation of mitochondrial β-oxidation enzymes.