The impact of SIRT3 on mitochondrial function and neuroinflammation in Alzheimer disease
10.3969/j.issn.1002-0152.2025.07.009
- VernacularTitle:SIRT3对阿尔茨海默病线粒体和神经炎症的影响
- Author:
Mengling LI
1
;
Xiaopeng TONG
;
Jie YAN
Author Information
1. 陕西省咸阳市西藏民族大学医学院(咸阳 712082)
- Publication Type:Journal Article
- Keywords:
Alzheimer disease;
SIRT3;
Mitochondria;
Neuroinflammation;
Specific agonists;
Therapeutic inter-ventions
- From:
Chinese Journal of Nervous and Mental Diseases
2025;51(7):437-443
- CountryChina
- Language:Chinese
-
Abstract:
This article systematically reviews the regulatory mechanism of SIRT3,an important mitochondrial deacetylase,in the pathogenesis of Alzheimer disease(AD).As a major mitochondrial deacetylase,SIRT3 participates in cerebral energy metabolism,neuroinflammation,and mitochondrial quality control by regulating mitochondrial protein functions.During the pathological process of AD,the downregulated expression of SIRT3 can induce hyperacetylation of mitochondrial proteins.This not only leads to mitochondrial dysfunction(such as impaired ATP synthesis and excessive reactive oxygen species production)but also impairs mitochondrial quality control mechanisms such as mitophagy and fusion/fission balance,thereby promoting mitochondrial damage.In addition,SIRT3 deficiency can activate neuroinflammatory pathways,prompting the release of inflammatory factors and further exacerbating neuronal damage.Future research will aim to undercover the detailed protective mechanisms of SIRT3 in AD,validate its feasibility as a therapeutic target for AD,and develop specific agonists,providing a theoretical basis for the intervention strategies of AD.
