耐力运动诱导的组织素甲基化修饰涉及骨肌肉纤维类型转换和线粒体生物发生
Jialin Li1, Sheng Zhang1,2, Can Li1,3
1Tianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin, 301617, China.
Scientific reports
|September 10, 2024
概括
耐力运动通过改变组织组织蛋白甲基化来促进快速到缓慢的肌肉纤维过渡,增强线粒体功能. 这种表观遗传转变是由反应性氧物种/AMPK途径介导的,这对于肌肉适应至关重要.
科学领域:
- 运动生理学 运动生理学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 骨肌肉生物学 骨肌肉生物学
背景情况:
- 骨肌肉表现出纤维异质性,具有明显的代谢特性.
- 众所周知,耐力运动可以促进快速动到慢速动的肌肉纤维过渡.
研究的目的:
- 在运动诱导的纤维类型转换过程中发现一种新的表观遗传机制,将肌肉收缩特性与代谢能力联系起来.
- 研究活性氧物种 (ROS) 和AMP激活蛋白激酶 (AMPK) 在运动调节的表观遗传修饰和肌肉纤维类型变化中的作用.
主要方法:
- 在大鼠中进行了为期8周的耐力运动方案,分析了胃肌中PGC-1α和肌重链 (MHC) 异型体的基因组甲基化.
- 在实验室研究中,使用与罗诺治疗的小鼠C2C12神经管来研究ROS/AMPK通路和基因素甲基化酶.
- 米托金 (MitoQ) 治疗,以确认ROS在线粒体生物发生和肌肉纤维类型合中的作用.
主要成果:
- 耐力炼诱导了组织素甲基化重塑,增加了线粒体生物发生,并将慢的纤维比率转移到快的纤维比率.
- 轮激活了ROS/AMPK通路和基因素甲基化酶,促进了线粒体生物发生和减缓MHC异型表达.
- 对于将线粒体生物发生与肌肉纤维类型适应相结合,ROS信号传递至关重要.
结论:
- 耐力运动通过重塑组质子甲基化来促进快速到缓慢的肌肉纤维过渡,将线粒体生物发生与缓慢的MHC异型表达联系起来.
- ROS/AMPK通路涉及到调解运动诱导的组织蛋白甲基化和随后的肌肉纤维类型适应.
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