Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice.

By N. Sundaresan, Madhu Gupta, Gene Kim, Senthilkumar B. Rajamohan, Ayman Isbatan, Mahesh P. Gupta. Journal of Clinical Investigation, 2009

1,016 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ce8f22fecdf27277a9a87f1799c774703d599b7d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Geriatrics and Gerontology

1. M. Haigis
2. E. Verdin
3. Wei Yu
4. S. Manolagas
5. Danica Chen
6. J. Vann
7. Lydia W. S. Finley
8. W. Hallows

In Molecular Biology

1. Arkaitz Carracedo
2. E. Verdin
3. P. Pandolfi
4. P. Moreira
5. Jiangwen Zhang
6. S. Manolagas
7. Lydia W. S. Finley
8. J. Denu

In Physiology

1. E. Verdin
2. M. Haigis
3. Arkaitz Carracedo
4. Wei Yu
5. S. Manolagas
6. Danica Chen
7. J. Vann
8. Lydia W. S. Finley

Citations in the corpus

• Sirt3 Mediates Reduction of Oxidative Damage and Prevention of Age-related Hearing Loss under Caloric Restriction (2010, background): “Sirt3 Enhances the Mitochondrial Glutathione Antioxidant Defense System in Response to CR A previous study has shown that overexpression of Sirt3 increased mRNA expression of the antioxidant genes manganese superoxide dismutase (MnSOD) and catalase (Cat) in primary cardiomyocytes and that Sirt3 / pr”
• Sirtuin 3, a New Target of PGC-1α, Plays an Important Role in the Suppression of ROS and Mitochondrial Biogenesis (2010, background): “Another recent study reported that SIRT3 can deacetylate Foxo3a to activate its target gene SOD2 [27,29].”
• Calorie restriction reduces oxidative stress by SIRT3-mediated SOD2 activation. (2010, background): “Notably, SIRT3 has been shown to protect mice from developing cancer and cardiac hypertrophy (Kim et al., 2010; Sundaresan et al., 2009).”
• From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “The importance of the latter mechanism has been recently highlighted by evidence that augmentation of FoxO3a-dependent MnSOD and catalase expression in mice by SIRT3 decreased cellular levels of ROS and thereby protected the mouse heart from cardiac hypertrophy (329).”
• NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential (2020, background): “574 As a negative regulator in cardiac hypertrophy, SIRT3 protects the heart by inhibiting intracellular ROS.140 Mice lacking SIRT3 become more sensitive to the stimulation of several pharmacological or non-pharmacological stressors, showing symptoms, such as fibrosis, cardiac hypertrophy and high m”
• The Role of Sirtuins in Antioxidant and Redox Signaling (2017, background): “For example, SIRT3 has been shown to activate isocitrate dehydrogenase (IDH2), SOD2, and CAT, all key enzymes in reducing the cellular burden of ROS (93, 154, 156).”
• SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization (2011, background): “Because SIRT3 is a well-known inhibitor of ROS (Kawamura et al., 2010; Kim et al., 2010; Kong et al., 2010; Sundaresan et al., 2009), we hypothesized that increased ROS in SIRT3-deficient cells would contribute to the inhibition of the PHDs.”