下调和上调
肌萎缩
骨骼肌
萎缩
肌肉萎缩
内分泌学
泛素
内科学
肌肉肥大
FOXO3公司
生物
蛋白质降解
福克斯O1
基因剔除小鼠
化学
细胞生物学
蛋白激酶B
医学
信号转导
生物化学
基因
受体
作者
Halimulati Abuduwaili,Kyoko Kamoshita,Kiyo‐aki Ishii,Kenta Takahashi,Tuerdiguli Abuduyimiti,Qifang Li,Yuki Isobe,Hisanori Goto,Yujiro Nakano,Yumie Takeshita,Hiroaki Takayama,Kenichi Harada,Toshinari Takamura
出处
期刊:American Journal of Physiology-endocrinology and Metabolism
[American Physiological Society]
日期:2023-06-01
卷期号:324 (6): E542-E552
被引量:1
标识
DOI:10.1152/ajpendo.00270.2022
摘要
The quality of skeletal muscle is maintained by a balance between protein biosynthesis and degradation. Disruption in this balance results in sarcopenia. However, its underlying mechanisms remain underinvestigated. Selenoprotein P (SeP; encoded by Selenop in mice) is a hepatokine that is upregulated in type 2 diabetes and aging and causes signal resistances via reductive stress. We created immobilized muscle atrophy model in Selenop knockout (KO) mice. Immobilization (IMM) significantly reduced cross-sectional areas and the size of skeletal muscle fibers, which were ameliorated in KO mice. IMM upregulated the genes encoding E3 ubiquitin ligases and their upstream FoxO1, FoxO3, and KLF15 transcription factors in the skeletal muscle, which were suppressed in KO mice. These findings suggest a possible involvement of SeP-mediated reductive stress in physical inactivity-mediated sarcopenia, which may be a therapeutic target against sarcopenia.NEW & NOTEWORTHY Selenoprotein P (SeP) is a hepatokine that is upregulated in type 2 diabetes and aging and causes signal resistances via reductive stress. Immobilization (IMM) significantly reduced skeletal muscle mass in mice, which was prevented in SeP knockout (KO) mice. IMM-induced Foxos/KLF15-atrogene upregulation was suppressed in the skeletal muscle of KO mice. These findings suggest that SeP-mediated reductive stress is involved in and may be a therapeutic target for physical inactivity-mediated muscle atrophy.
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