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有氧加强力运动减轻了通过HDAC4/FoxO3a途径通过德甲诱导的骨肌肉缩

Dehuan Liang¹, Danni Wang¹, Xinyue Zheng¹

¹Department of Rehabilitation, School of Medical Technology, Tianjin Medical University, Tianjin 300070, China.

Cellular signalling

|December 28, 2024

概括

运动通过抑制HDAC4/FoxO3a通路来对抗德克萨米他诱导的肌肉缩. 运动干预改善了肌肉质量和功能,表明HDAC4作为治疗点.

科学领域:

肌肉生理学肌肉生理学
分子生物学分子生物学
运动科学运动科学

背景情况:

德克萨米他 (Dex) 诱导肌肉缩,其特点是变化的表型和特基表达.
在德克斯诱导的肌肉缩中,基斯脱乙酶4 (HDAC4) 被上调调节.
需要阐明HDAC4在运动中介保护肌肉损失中的作用.

研究的目的:

调查身体炼减轻甲诱导的肌肉缩的机制.
为了确定HDAC4/FoxO3a途径在Dex诱导的肌肉衰竭中的参与.
探索运动作为肌肉缩的潜在干预措施.

主要方法:

在C2C12细胞和小鼠中建立了Dex诱导的肌肉缩模型.
使用RT-PCR,西式涂抹,免疫沉和免疫光染色.
服用HDAC4抑制剂 (Tasquinimod) 并进行了为期6周的运动干预.

主要成果:

在用Dex治疗的肌肉细胞和小鼠中证实了HDAC4上调.
抑制HDAC4增加了肌管直径和融合指数,减少了Atrogin-1和MuRF1的表达.
在接受德克斯治疗的小鼠中,运动干预改善了身体脂肪,高胰岛素血症,肌肉质量和功能.
HDAC4脱乙基化FoxO3a,促进Atrogin-1/MuRF1的表达和肌肉缩.

结论:

运动通过抑制HDAC4/FoxO3a通路来减轻肌肉缩.
使用Tasquinimod抑制HDAC4可以防止Dex诱导的肌肉衰竭.
通过运动,HDAC4代表了一种潜在的治疗标,用于通过运动对抗德克萨米他诱导的肌肉缩.

关键词:

有氧运动加上阻力运动.德克萨米他是一种在FoxO3a中使用.在 HDAC4 中,HDAC4 是骨肌肉缩骨肌肉缩

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