Loss of SELENOW aggravates muscle loss with regulation of protein synthesis and the ubiquitin-proteasome system
文献类型： 外文期刊
作者： Yang, Jia-Cheng 1 ; Liu, Meng 1 ; Huang, Rong-Hui 1 ; Zhao, Ling 1 ; Niu, Qin-Jian 1 ; Xu, Ze-Jing 1 ; Wei, Jin-Tao 2 ; Lei, Xin Gen 3 ; Sun, Lv-Hui 1 ;
作者机构： 1.Huazhong Agr Univ, Coll Anim Sci & Technol, Frontiers Sci Ctr Anim Breeding & Sustainable Prod, State Key Lab Agr Microbiol,Hubei Hongshan Lab, Wuhan 430070, Hubei, Peoples R China
2.Hubei Acad Agr Sci, Inst Anim Husb & Vet Sci, Wuhan 430064, Peoples R China
3.Cornell Univ, Dept Anim Sci, Ithaca, NY 14853 USA
期刊名称：SCIENCE ADVANCES （ 影响因子：12.5； 五年影响因子：14.1 ）
ISSN： 2375-2548
年卷期： 2024 年 10 卷 38 期
页码：
收录情况： SCI
摘要： Sarcopenia is characterized by accelerated muscle mass and function loss, which burdens and challenges public health worldwide. Several studies indicated that selenium deficiency is associated with sarcopenia; however, the specific mechanism remains unclear. Here, we demonstrated that selenoprotein W (SELENOW) containing selenium in the form of selenocysteine functioned in sarcopenia. SELENOW expression is up-regulated in dexamethasone (DEX)-induced muscle atrophy and age-related sarcopenia mouse models. Knockout (KO) of SELENOW profoundly aggravated the process of muscle mass loss in the two mouse models. Mechanistically, SELENOW KO suppressed the RAC1-mTOR cascade by the interaction between SELENOW and RAC1 and induced the imbalance of protein synthesis and degradation. Consistently, overexpression of SELENOW in vivo and in vitro alleviated the muscle and myotube atrophy induced by DEX. SELENOW played a role in age-related sarcopenia and regulated the genes associated with aging. Together, our study uncovered the function of SELENOW in age-related sarcopenia and provides promising evidence for the prevention and treatment of sarcopenia.
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