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. 2022 Sep 7;24(5):662. doi: 10.3892/etm.2022.11598

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Copyright: © Jiang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Summary of the results. Lipopolysaccharide-activated microglia release a variety of inflammatory factors that can result in oxidative stress damage and promote the apoptosis of dopaminergic neurons. SIRT3 overexpression in dopaminergic neurons can inhibit apoptosis induced by the excessive microglia activation. The mechanism of this action may be associated with the expression of SIRT3 promoting mitophagy, restoring mitochondrial dysfunction and reducing ROS production, thereby inhibiting NLRP3 inflammasome activation. SIRT3, sirtuin 3; ROS, reactive oxygen species; NLRP3, nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing protein 3.