LncEDCH1 improves mitochondrial function to reduce muscle atrophy by interacting with SERCA2
文献类型： 外文期刊
作者： Cai, Bolin 1 ; Ma, Manting 1 ; Zhang, Jing 1 ; Wang, Zhijun 1 ; Kong, Shaofen 1 ; Zhou, Zhen 1 ; Lian, Ling 4 ; Zhang, Jiannan 6 ; Li, Juan 6 ; Wang, Yajun 6 ; Li, Hongmei 1 ; Zhang, Xiquan 1 ; Nie, Qinghua 1 ;
作者机构： 1.South China Agr Univ, Coll Anim Sci, Lingnan Guangdong Lab Modern Agr, Guangzhou 510642, Guangdong, Peoples R China
2.South China Agr Univ, Coll Anim Sci, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Guangdong, Peoples R China
3.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Guangdong, Peoples R China
4.China Agr Univ, Coll Anim Sci & Technol, Natl Engn Lab Anim Breeding, Beijing 100193, Peoples R China
5.China Agr Univ, Coll Anim Sci & Technol, MOA Key Lab Anim Genet & Breeding, Beijing 100193, Peoples R China
6.Sichuan Univ, Coll Life Sci, Key Lab Bioresources & Ecoenvironm, Minist Educ, Chengdu 610065, Peoples R China
期刊名称：MOLECULAR THERAPY-NUCLEIC ACIDS （ 影响因子：10.183； 五年影响因子：9.043 ）
ISSN： 2162-2531
年卷期： 2022 年 27 卷
页码：
收录情况： SCI
摘要： Skeletal muscle is a regulator of the body's energy expenditure and metabolism. Abnormal regulation of skeletal muscle-specific genes leads to various muscle diseases. Long non-coding RNAs (lncRNAs) have been demonstrated to play important roles in muscle growth and muscle atrophy. To explore the potential function of muscle-associated lncRNA, we analyzed our previous RNA-sequencing data and selected the lncRNA (LncEDCH1) as the research object. In this study, we report that LncEDCH1 is specifically enriched in skeletal muscle, and its transcriptional activity is positively regulated by transcription factor SP1. LncEDCH1 regulates myoblast proliferation and differentiation in vitro. In vivo, LncEDCH1 reduces intramuscular fat deposition, activates slow-twitch muscle phenotype, and inhibits muscle atrophy. Mechanistically, LncEDCH1 binds to sarcoplasmic/ER calcium ATPase 2 (SERCA2) protein to enhance SERCA2 protein stability and increase SERCA2 activity. Meanwhile, LncEDCH1 improves mitochondrial efficiency possibly through a SERCA2-mediated activation of the AMPK pathway. Our findings provide a strategy for using LncEDCH1 as an effective regulator for the treatment of muscle atrophy and energy metabolism.
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