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Angiotensin 2 AND Sirt3

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https://www.readbyqxmd.com/read/28684630/sirt3-impairment-and-sod2-hyperacetylation-in-vascular-oxidative-stress-and-hypertension
#1
Anna E Dikalova, Hana A Itani, Rafal R Nazarewicz, William G McMaster, Charles R Flynn, Roman Uzhachenko, Joshua P Fessel, Jorge L Gamboa, David G Harrison, Sergey I Dikalov
RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels. Sirt3 impairment reduces the activity of a key mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2) because of hyperacetylation. OBJECTIVE: In this study, we examined whether the loss of Sirt3 activity increases vascular oxidative stress because of SOD2 hyperacetylation and promotes endothelial dysfunction and hypertension...
August 18, 2017: Circulation Research
https://www.readbyqxmd.com/read/28579116/sirt3-prevents-angiotensin-ii-induced-renal-tubular-epithelial-mesenchymal-transition-by-ameliorating-oxidative-stress-and-mitochondrial-dysfunction
#2
Ping He, Zhuoming Li, Zhongbao Yue, Hui Gao, Guoshuai Feng, Panxia Wang, Yi Huang, Wenwei Luo, Huiqi Hong, Liying Liang, Shaorui Chen, Peiqing Liu
Silent mating type information regulation 2 homolog 3 (SIRT3) is a major protective mediator that ameliorates oxidative stress and mitochondrial dysfunction, which are associated with the pathogenesis of epithelial-mesenchymal transition (EMT). The present study was aimed to investigate the potential role of SIRT3 in renal tubular EMT both in vitro and in vivo. Firstly, we showed that the expression of SIRT3 was repressed in angiotensin II-induced EMT. SIRT3 deficiency triggered EMT response, while over-expression of SIRT3 attenuated EMT response...
June 1, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28296029/cd38-promotes-angiotensin-ii-induced-cardiac-hypertrophy
#3
Xiao-Hui Guan, Xuan Hong, Ning Zhao, Xiao-Hong Liu, Yun-Fei Xiao, Ting-Tao Chen, Li-Bin Deng, Xiao-Lei Wang, Jian-Bin Wang, Guang-Ju Ji, Mingui Fu, Ke-Yu Deng, Hong-Bo Xin
Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H2 O2 -induced injury and hypoxia/reoxygenation-induced injury. In addition, we also found that CD38 knockout mice protected heart from ischaemia reperfusion injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway. However, the role of CD38 in cardiac hypertrophy is not explored...
August 2017: Journal of Cellular and Molecular Medicine
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