Sirtuin 3 (SIRT3), a mitochondrial deacetylase expressed preferentially in high-metabolic-demand tissues including the brain, requires NAD as a cofactor for catalytic activity. It regulates various processes such as energy homeostasis, redox balance, mitochondrial quality control, mitochondrial unfolded protein response, biogenesis, dynamics and mitophagy by altering protein acetylation status. Reduced SIRT3 expression or activity causes hyperacetylation of hundreds of mitochondrial proteins, which has been linked with neurological abnormalities, neuro-excitotoxicity and neuronal cell death. A body of evidence has suggested, SIRT3 activation as a potential therapeutic modality for age-related brain abnormalities and neurodegenerative disorders.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.drudis.2023.103583 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Synergistic effects of PS-NPs and Cd on ovarian toxicity in adolescent rats: Ferroptosis by induction of mitochondrial redox imbalance via the SIRT3-SOD2/Gpx4 pathway.
Ecotoxicol Environ Saf
December 2024
The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330000, China. Electronic address:
Nanoplastics (NPs) are an emerging class of pollutants. They can act as a"Trojan horse" to change the bioavailability and toxicity of heavy metals in the environment. However, research on the combined toxicity of heavy metals and NPs is scarce, especially during the critical developmental period of adolescence.
View Article and Find Full Text PDFBrazilin alleviates acute lung injury via inhibition of ferroptosis through the SIRT3/GPX4 pathway.
Apoptosis
December 2024
Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215000, Jiangsu, China.
Ferroptosis is a novel type of programmed cell death dependent on iron and is characterized by the accumulation of lipid peroxides, which is involved in acute lung injury (ALI). Brazilin, an organic compound known for its potent antioxidant and anti-inflammatory properties, has not been thoroughly studied for its potential impact on lipopolysaccharide (LPS)-induced ALI. Here, we found that pretreatment of brazilin mitigated LPS-induced lung injury and inflammation by inhibiting mitochondrial oxidative stress and ferroptosis, both in vivo and in vitro.
View Article and Find Full Text PDFExercise training alleviates neuronal apoptosis and re-establishes mitochondrial quality control after cerebral ischemia by increasing SIRT3 expression.
Cell Biol Toxicol
December 2024
Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Existing evidence indicates that exercise training can enhance neural function by regulating mitochondrial quality control (MQC), which can be impaired by cerebral ischemia, and that sirtuin-3 (SIRT3), a protein localized in mitochondria, is crucial in maintaining mitochondrial functions. However, the relationship among exercise training, SIRT3, and MQC after cerebral ischemia remains obscure. This study attempted to elucidate the relationship among exercise training, SIRT3 and MQC after cerebral ischemia in rats.
View Article and Find Full Text PDF[Ginsenoside Rg_1 modulates ATP5A1 deacetylation via SIRT3 to attenuate hypoxia/reoxygenation injury in HL-1 cardiomyocytes].
Zhongguo Zhong Yao Za Zhi
October 2024
Institute of Basic Medicine, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China National Clinical Research Center for Chinese Medicine Cardiology Beijing 100091, China.
This study investigated the mechanism by which ginsenoside Rg_(1 )attenuates hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes by inhibiting the acetylation of ATP synthase subunit alpha(ATP5A1) through silent information regulator 3(SIRT3). In this study, an H/R injury model was constructed by hypoxia for 6 h and reoxygenation for 2 h in HL-1 cardiomyocytes. First, the optimal effective concentration of ginsenoside Rg_1 was determined using a cell viability assay kit.
View Article and Find Full Text PDF7-Hydroxy-3-(4'-methoxyphenyl) coumarin (C12) attenuates bleomycin-induced acute lung injury and fibrosis through activation of SIRT3.
Biochem Pharmacol
December 2024
Department of Biological Sciences (Pharmacology & Toxicology), National Institute of Pharmaceutical Education and Research (NIPER) Hyderabad, Telangana 500037, India. Electronic address:
Silent mating-type information regulation 2 homology 3 (SIRT3) is a member of the sirtuins family expressed in mitochondria performs deacetylation of metabolic enzymes and promotes longevity. 7-hydroxy-3-(4'-methoxyphenyl) coumarin (C12) is a small molecule first ever known for its direct activation of SIRT3. SIRT3 performs its function by balancing the redox system by activating manganese superoxide dismutase (MnSOD) and 8-Oxoguanine glycosylase (OGG1).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!