运动训练通过抑制YTHDF2来降低乳和预防心肌缺血-再输损伤
Gui-E Xu1,2, Pujiao Yu3, Yuxue Hu1,2
1Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Life Science, Shanghai University, Nantong, 226011, China.
Basic research in cardiology
|April 2, 2024
概括
运动通过改变蛋白质乳糖化和RNA结合蛋白YTHDF2.2的影响心脏功能. 这项研究揭示了调节心肌细胞适应运动的新机制,以及心脏病的潜在治疗点.
科学领域:
- 心血管生理学心血管生理学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 运动可以增强心脏功能和新陈代谢,但其对蛋白质乳酸和功能相关性的影响尚不清楚.
- 乳酸盐是一种关键的代谢副产品,越来越多地被认为具有超出能源供应的调节作用.
- 翻译后的修改,包括乳糖化,对于细胞信号传递和适应至关重要.
研究的目的:
- 为了研究蛋白质乳糖化在运动诱导的心脏适应中的作用.
- 阐明RNA结合蛋白YTHDF2在心肌细胞调节中的功能意义.
- 为了探索乳酸,乳化,YTHDF2和心脏对压力的反应之间的相互作用.
主要方法:
- 对心肌细胞中蛋白质乳糖化水平的分析.
- 通过基因操纵和基于细胞的测试来研究YTHDF2的功能.
- 使用氧气葡萄糖剥夺/再氧化 (OGD/R) 和缺血/再输血模型.
- 评估心肌细胞大小,细胞亡和心脏重塑.
主要成果:
- 乳酸盐通过增加蛋白质乳酸和细胞内YTHDF2水平来调节心肌细胞的变化.
- YTHDF2的内在障碍区域,而不是它的RNA结合活性,对于通过G3BP1.1.R调节细胞大小和OGD/R诱导的细胞亡至关重要.
- 降低YTHDF2的调节对于运动引起的生理性心脏缩至关重要,其抑制可以减轻心脏损伤和重塑.
结论:
- 这项研究确定了乳酸,乳酸和m6ARNA读者YTHDF2在心肌细胞适应运动中的联系.
- 涉及YTHDF2和G3BP1的新型转录后调节机制控制心肌细胞的反应.
- 向乳化或YTHDF2/G3BP1轴为心血管疾病提供了潜在的治疗策略.
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