SIRT3 KO mice show higher visceral fibrosis with aging and increased blood pressure compared to wild-type controls. In addition, SIRT3 deficiency induces human cardiac fibroblast-to-myofibroblast differentiation, as SIRT3-depleted human cardiac fibroblasts showcased an increased myofibroblast marker expression.

Accumulating evidence suggests that SIRT3 plays a critical role in protecting the heart from cardiac hypertrophy, cardiac dysfunction associated with heart failure, and in the protection of cardiac cells from stress-mediated cell death.

Sirtuin 3 (SIRT3) is one of the most prominent deacetylases that can regulate acetylation levels in mitochondria, which are essential for eukaryotic life and inextricably linked to the metabolism of multiple organs.

Sep 13, 2021 · Sirt3 knockout mice were susceptible to hyper-acetylated mitochondrial proteins and to severe renal fibrosis. The activation of SIRT3 by honokiol ameliorated acetylation and prevented renal...

Oct 18, 2024 · We quantitatively analyzed the Kla and Kac proteomes in wildtype (WT), SIRT1 knockout (KO), and SIRT3 KO HepG2 cells, successfully identifying 8075 Kla sites and 3515 Kac sites, respectively. Furthermore, we investigated the Kla and Kac substrates specifically regulated by SIRT1 or SIRT3.

Mar 1, 2016 · We found that Sirt3 knockout (KO) mice with age develop tissue fibrosis of multiple organs, including heart, liver, kidney, and lungs but not whole-body SIRT3-overexpressing mice.

Aug 20, 2023 · Sirt3 -KO promoted oxidative stress and energetics defects caused by MWI, whereas cardiac-specific SIRT3 overexpression inhibited these detrimental effects and rescued heart dysfunction. Mechanistically, we demonstrated that Sirt3 activated the AMPK cascade in the hearts of eRIC mice.

May 2, 2024 · Wild-type and SIRT3 knockout (KO) mice were randomly assigned to receive cyclosporine A or olive oil. Furthermore, SIRT3 activator, honokiol, was treated alongside CsA to wild type mice. Our...

In this study, using Sirt3 knockout (Sirt3-/-) mice, we sought to establish whether Sirt3 deficiency affected life span, an endpoint that has never been tested formally in mammals, and uncover the mechanisms involved in organ damage associated with aging.

Endothelial SIRT3-KO impairs expression of hypoxia-induced apelin, glucose transporters GLUT1 and GLUT4, and phosphofructokinase-2/fructose-2, 6-bisphosphatase-3 in endothelial cells—thereby disrupting glucose transport to cardiomyocytes (123).