Sirt2 ablation exacerbates Sod1 knockout-induced progeroid phenotype in mice.

Anke Geng, Xiaona Wang, Zhenkai Wu, Zhihao Liu, Xiao Huang, Xiyue Wang, Xiaoxiang Sun, Yingjie Wang, Jiayu Chen, Ying Jiang, Huanyin Tang, Zhiyong Mao

Shanghai Key Laboratory of Maternal Fetal Medicine, Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.Shanghai Key Laboratory of Maternal Fetal Medicine, Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. · pubmed

Paper

Abstract

The free radical theory of aging suggests that oxidative stress from free radicals contributes to aging. While free radicals cause DNA damage and cellular dysfunction, they also regulate essential signaling pathways. This duality complicates direct testing of the theory in mice, as demonstrated by the minor lifespan impact of Sod1 knockout. We hypothesize that base excision repair mechanisms, that involve SIRT2, a longevity-associated SIRTUIN family member, may mitigate excessive free radical effects. Our study found that Sirt2

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that SIRT2 ablation exacerbates the progeroid phenotype in Sod1 knockout mice, suggesting a role for SIRT2 in mitigating oxidative stress effects related to aging. This research is relevant as it explores mechanisms that may influence aging processes and longevity through the lens of oxidative stress and DNA repair.

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