The Functional Role of Long Non-Coding RNA in Myogenesis and Skeletal Muscle Atrophy

被引：18

作者：

Hitachi, Keisuke ^{[1
]}

Honda, Masahiko ^{[2
]}

Tsuchida, Kunihiro ^{[1
]}

机构：

[1] Fujita Hlth Univ, Inst Comprehens Med Sci ICMS, Div Therapies Intractable Dis, Toyoake, Aichi 4701192, Japan

[2] Kindai Univ, Fac Med, Dept Biochem, Osakasayama 5898511, Japan

来源：

CELLS | 2022年 / 11卷 / 15期

关键词：

long non-coding RNA; Myoparr; skeletal muscle atrophy; cachexia; sarcopenia; CELL-PROLIFERATION; UBIQUITIN LIGASES; UNIQUE FEATURES; GENE; DIFFERENTIATION; EXPRESSION; MICE; MYOD; MASS; MUTATION;

D O I：

10.3390/cells11152291

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Skeletal muscle is a pivotal organ in humans that maintains locomotion and homeostasis. Muscle atrophy caused by sarcopenia and cachexia, which results in reduced muscle mass and impaired skeletal muscle function, is a serious health condition that decreases life longevity in humans. Recent studies have revealed the molecular mechanisms by which long non-coding RNAs (lncRNAs) regulate skeletal muscle mass and function through transcriptional regulation, fiber-type switching, and skeletal muscle cell proliferation. In addition, lncRNAs function as natural inhibitors of microRNAs and induce muscle hypertrophy or atrophy. Intriguingly, muscle atrophy modifies the expression of thousands of lncRNAs. Therefore, although their exact functions have not yet been fully elucidated, various novel lncRNAs associated with muscle atrophy have been identified. Here, we comprehensively review recent knowledge on the regulatory roles of lncRNAs in skeletal muscle atrophy. In addition, we discuss the issues and possibilities of targeting lncRNAs as a treatment for skeletal muscle atrophy and muscle wasting disorders in humans.

引用

页数：24

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