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RAS AND Sirt3

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https://www.readbyqxmd.com/read/26517140/the-role-of-sirt3-in-mediating-cardioprotective-effects-of-ras-inhibition-on-cardiac-ischemia-reperfusion
#1
REVIEW
Sabzali Javadov, Nelson Escobales
Cardiac ischemia-reperfusion stimulates the renin-angiotensin system (RAS) associated with elevated levels of circulating angiotensin II. Numerous studies demonstrate that the antagonist for the angiotensin II type 1 receptor, losartan improves cardiac function in animal models of ischemia-reperfusion. Molecular mechanisms of the cardioprotective effects of RAS inhibitors on cardiac ischemia-reperfusion remain poorly understood, and are not associated with the anti-hypertensive action of these drugs. This Commentary focuses on the study published in the Journal of Pharmacy and Pharmaceutical Sciences, 2015, 18:112-123, that elucidates the role of SIRT3 in the cardioprotective action of losartan against ischemic-reperfusion injury...
2015: Journal of Pharmacy & Pharmaceutical Sciences: a Publication of the Canadian Society for Pharmaceutical Sciences
https://www.readbyqxmd.com/read/25877446/losartan-protects-the-heart-against-ischemia-reperfusion-injury-sirtuin3-involvement
#2
Mohsen Sharifi Klishadi, Farideh Zarei, Seyyed Hassan Hejazian, Ali Moradi, Mahdieh Hemati, Fatemeh Safari
PURPOSE: Sirtuin-3 (SIRT3) deacetylase protects the heart against oxidative stress via survival factors upregulation. Clinical and experimental studies have demonstrated that activation of systemic and local renin-angiotensin system (RAS) is implicated in ischemia-induced cardiac injury. However, the relation between RAS and SIRT3 in pathophysiology of myocardial ischemia reperfusion is unknown. In this study, the cardiac transcription and expression of SIRT3 levels was examined in response to ischemia reperfusion in untreated and losartan treated rats...
2015: Journal of Pharmacy & Pharmaceutical Sciences: a Publication of the Canadian Society for Pharmaceutical Sciences
https://www.readbyqxmd.com/read/25320353/combination-of-ace-inhibitor-with-nicorandil-provides-further-protection-in-chronic-kidney-disease
#3
Takeshi Shiraishi, Yoshifuru Tamura, Kei Taniguchi, Masato Higaki, Shuko Ueda, Tomoko Shima, Michito Nagura, Takahiko Nakagawa, Richard J Johnson, Shunya Uchida
An inhibition in the renin-angiotensin system (RAS) is one of the most widely used therapies to treat chronic kidney disease. However, its effect is occasionally not sufficient and additional treatments may be required. Recently, we reported that nicorandil exhibited renoprotective effects in a mouse model of diabetic nephropathy. Here we examined if nicorandil can provide an additive protection on enalapril in chronic kidney disease. Single treatment with either enalapril or nicorandil significantly ameliorated glomerular and tubulointerstitial injury in the rat remnant kidney while the combination of these two compounds provided additive effects...
December 15, 2014: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/24955214/sod1-an-unexpected-novel-target-for-cancer-therapy
#4
REVIEW
Luena Papa, Giovanni Manfredi, Doris Germain
Cancer cells have elevated levels of reactive oxygen species (ROS), which are generated in majority by the mitochondria. In the mitochondrial matrix, the manganese dismutase SOD2 acts as a major anti-oxidant enzyme. The deacetylase SIRT3 regulates the activity of SOD2. Recently, SIRT3 was reported to be decreased in 87% of breast cancers, resulting therefore in a decrease in the activity of SOD2 and an elevation in ROS. In addition to SIRT3, we recently reported that SOD2 itself is down-regulated in breast cancer cell lines upon activation of oncogenes, such as Ras...
April 2014: Genes & Cancer
https://www.readbyqxmd.com/read/24448804/sod2-to-sod1-switch-in-breast-cancer
#5
Luena Papa, Mary Hahn, Ellen L Marsh, Bradley S Evans, Doris Germain
Cancer cells are characterized by elevated levels of reactive oxygen species, which are produced mainly by the mitochondria. The dismutase SOD2 localizes in the matrix and is a major antioxidant. The activity of SOD2 is regulated by the deacetylase SIRT3. Recent studies indicated that SIRT3 is decreased in 87% of breast cancers, implying that the activity of SOD2 is compromised. The resulting elevation in reactive oxygen species was shown to be essential for the metabolic reprograming toward glycolysis. Here, we show that SOD2 itself is down-regulated in breast cancer cell lines...
February 28, 2014: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/23396452/ang-ii-causes-insulin-resistance-and-induces-cardiac-metabolic-switch-and-inefficiency-a-critical-role-of-pdk4
#6
Jun Mori, Osama Abo Alrob, Cory S Wagg, Robert A Harris, Gary D Lopaschuk, Gavin Y Oudit
The renin-angiotensin system (RAS) may alter cardiac energy metabolism in heart failure. Angiotensin II (ANG II), the main effector of the RAS in heart failure, has emerged as an important regulator of cardiac hypertrophy and energy metabolism. We studied the metabolic perturbations and insulin response in an ANG II-induced hypertrophy model. Ex vivo heart perfusion showed that hearts from ANG II-treated mice had a lower response to insulin with significantly reduced rates of glucose oxidation in association with increased pyruvate dehydrogenase kinase 4 (PDK4) levels...
April 15, 2013: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/22283774/role-of-renin-angiotensin-system-in-inflammation-immunity-and-aging
#7
REVIEW
Luciano S A Capettini, Fabrizio Montecucco, Francois Mach, Nikos Stergiopulos, Robson A S Santos, Rafaela F da Silva
Recent data support the idea that the effects of RAS are not restricted to the cardiovascular and renal systems. Importantly, RAS modulates free radical production and the cellular synthesis of several molecules such as cytokines, chemokines and transcription factors. These functions reflect directly the RAS ability to modulate the cell growth, senescence and migration. Activation of the classic RAS, ACE/Ang II/AT1R, has been strictly related to down regulation of pro-survival genes (Nampt and Sirt3), increase in ROS production and pro-inflammatory cytokines and chemokines release, leading to cell senescence, inflammation and development of autoimmune dysfunctions...
2012: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/21172655/sirt3-mediated-deacetylation-of-evolutionarily-conserved-lysine-122-regulates-mnsod-activity-in-response-to-stress
#8
Randa Tao, Mitchell C Coleman, J Daniel Pennington, Ozkan Ozden, Seong-Hoon Park, Haiyan Jiang, Hyun-Seok Kim, Charles Robb Flynn, Salisha Hill, W Hayes McDonald, Alicia K Olivier, Douglas R Spitz, David Gius
Genetic deletion of the mitochondrial deacetylase sirtuin-3 (Sirt3) results in increased mitochondrial superoxide, a tumor-permissive environment, and mammary tumor development. MnSOD contains a nutrient- and ionizing radiation (IR)-dependent reversible acetyl-lysine that is hyperacetylated in Sirt3⁻/⁻ livers at 3 months of age. Livers of Sirt3⁻/⁻ mice exhibit decreased MnSOD activity, but not immunoreactive protein, relative to wild-type livers. Reintroduction of wild-type but not deacetylation null Sirt3 into Sirt3⁻/⁻ MEFs deacetylated lysine and restored MnSOD activity...
December 22, 2010: Molecular Cell
https://www.readbyqxmd.com/read/20129246/sirt3-is-a-mitochondria-localized-tumor-suppressor-required-for-maintenance-of-mitochondrial-integrity-and-metabolism-during-stress
#9
Hyun-Seok Kim, Krish Patel, Kristi Muldoon-Jacobs, Kheem S Bisht, Nukhet Aykin-Burns, J Daniel Pennington, Riet van der Meer, Phuongmai Nguyen, Jason Savage, Kjerstin M Owens, Athanassios Vassilopoulos, Ozkan Ozden, Seong-Hoon Park, Keshav K Singh, Sarki A Abdulkadir, Douglas R Spitz, Chu-Xia Deng, David Gius
The sirtuin gene family (SIRT) is hypothesized to regulate the aging process and play a role in cellular repair. This work demonstrates that SIRT3(-/-) mouse embryonic fibroblasts (MEFs) exhibit abnormal mitochondrial physiology as well as increases in stress-induced superoxide levels and genomic instability. Expression of a single oncogene (Myc or Ras) in SIRT3(-/-) MEFs results in in vitro transformation and altered intracellular metabolism. Superoxide dismutase prevents transformation by a single oncogene in SIRT3(-/-) MEFs and reverses the tumor-permissive phenotype as well as stress-induced genomic instability...
January 19, 2010: Cancer Cell
https://www.readbyqxmd.com/read/19652361/sirt3-blocks-the-cardiac-hypertrophic-response-by-augmenting-foxo3a-dependent-antioxidant-defense-mechanisms-in-mice
#10
Nagalingam R Sundaresan, Madhu Gupta, Gene Kim, Senthilkumar B Rajamohan, Ayman Isbatan, Mahesh P Gupta
Sirtuin 3 (SIRT3) is a member of the sirtuin family of proteins that promote longevity in many organisms. Increased expression of SIRT3 has been linked to an extended life span in humans. Here, we have shown that Sirt3 protects the mouse heart by blocking the cardiac hypertrophic response. Although Sirt3-deficient mice appeared to have normal activity, they showed signs of cardiac hypertrophy and interstitial fibrosis at 8 weeks of age. Application of hypertrophic stimuli to these mice produced a severe cardiac hypertrophic response, whereas Sirt3-expressing Tg mice were protected from similar stimuli...
September 2009: Journal of Clinical Investigation
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