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O-GlcNAcylation of SIRT1 Protects against Cold Stress-Induced Skeletal Muscle Damage via Amelioration of Mitochondrial Homeostasis

文献类型： 外文期刊

作者： Cao, Yu 1 ; Zhang, Meng 1 ; Li, Ye 2 ; Lu, Jingjing 1 ; Zhou, Wanhui 1 ; Li, Xiaoshuang 1 ; Shi, Hao 3 ; Xu, Bin 1 ; Li, Shize 1 ;

作者机构： 1.Heilongjiang Bayi Agr Univ, Coll Anim Sci & Vet Med, Daqing 163319, Peoples R China

2.Heilongjiang Acad Agr Sci, Branch Anim Husb & Vet, Sheep Dis Lab, Qiqihar 161005, Peoples R China

3.Virginia Polytech Inst & State Univ, Dept Anim & Poultry Sci, Blacksburg, VA 24061 USA

关键词： cold stress; skeletal muscle; metabolic homeostasis imbalance; SIRT1; O-GlcNAcylation

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：6.208； 五年影响因子：6.628 ）

ISSN：

年卷期： 2022 年 23 卷 23 期

页码：

收录情况： SCI

摘要： Cold stress disturbs cellular metabolic and energy homeostasis, which is one of the causes of stress-induced illnesses. O-GlcNAcylation is a nutrient-sensing pathway involved in a myriad of cellular processes. It plays a key role in metabolic homeostasis. Nevertheless, a specific sensing mechanism linking skeletal muscle to O-GlcNAcylation in cold stress is unknown. In this study, O-GlcNAcylation of SIRT1 was targeted to explore the mechanism of skeletal muscle adaptation to cold stress. Ogt mKO aggravated skeletal muscle fibrosis induced by cold stress. At the same time, Ogt gene deletion accelerated the homeostasis imbalance and oxidative stress of skeletal muscle mitochondria induced by cold stress. In vitro results showed that inhibition of SIRT1's O-GlcNAcylation accelerated mild hypothermia induced mitochondrial homeostasis in mouse myogenic cells (C2C12 cells). However, overexpression of SIRT1's O-GlcNAcylation improved the above phenomena. Thus, these results reveal a protective role of OGT-SIRT1 in skeletal muscle's adaptation to cold stress, and our findings will provide new avenues to combat stress-induced diseases.

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