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运动诱导的生理心肌缩后的抗高缩记忆是由长非编码RNAMhrt779介导的

Hairuo Lin¹, Yingqi Zhu¹, Cankun Zheng¹

¹Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Lab of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China (H.L., Y.Z., C.Z., D.H., S.M., L.C., Q.W., Z.C., J.X., Y.Y., X.H., M.K., J.B., Y.L.).

|March 24, 2021

概括

运动引起的生理性心肌缩 (PMH) 提供了对病理性压力的持久保护. 这种由Mhrt779 lncRNA介导的"记忆"效应,即使在PMH回归后,也会增强心脏抵抗力.

科学领域:

心脏病学
分子生物学
运动生理学

背景情况:

运动会导致心肌缩,这可能会对心血管产生长期益处.
之前的研究表明,病态缩的回归具有抗缩作用.
这项研究调查了PMH回归后是否存在抗缩记忆.

研究的目的:

要确定运动诱导的PMH是否会对病态心脏压力产生持久的抵抗力.
解释这种抗高性记忆的分子机制.

主要方法:

小鼠接受了游泳训练以诱导PMH,随后进行回归.
在PMH回归和对照小鼠中进行横向大动脉收缩.
分析了涉及lncRNA Mhrt779的心脏功能,重塑和分子途径.

主要成果:

经过运动预先调整的心脏在收缩后表现出降低的增大和改善的功能.
长非编码RNAMhrt779被上调,对保护作用至关重要.
Mhrt779与Brg1相互作用以抑制Hdac2/Akt/GSK3β通路.

结论:

运动诱导的PMH建立了抗高性记忆.
这种记忆增强了心脏对病理性压力的抵抗力.
通过Mhrt779/Brg1/Hdac2/Akt/GSK3β途径进行这种保护作用.

关键词:

长非编码的RNA 进行心脏衰竭过度增长

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