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LncRNA MIR217HG通过激活miR-138/THBS1通路来加剧压力过载诱导的心脏重塑

Xiang Nie¹, Rong Xie¹, Jiahui Fan¹

¹Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan 430030, China.

|November 28, 2023

概括

MIR217HG转录促进心脏重塑和纤维化,导致心脏衰竭. 它通过与miR-138/THBS1通路相互作用来激活这个过程,突出显示了一个新的治疗点.

科学领域:

心血管生物学心血管生物学
分子心脏病学分子心脏病学
基因规则基因规则

背景情况:

心脏缩和纤维化是心脏重塑和心力衰竭的关键驱动因素.
之前的研究已经确定了miRNA-217在压力过载引起的心脏缩中的作用.
在心脏重塑中,MIR217HG转录本身的功能以前是未知的.

研究的目的:

研究MIR217HG转录在心脏重塑中的作用.
阐明了MIR217HG在心脏中的功能背后的分子机制.

主要方法:

使用实时PCR和现场杂交,量化了MIR217HG表达.
病毒载体 (lentivirus,AAV) 具有心脏特异性促进体控制MIR217HG表达在体外和体内.
通过横向大动脉收缩 (TAC) 手术诱导心脏重塑,通过心声学和压力体积分析评估心脏结构和功能.

主要成果:

在心力衰竭患者中,MIR217HG表达升高.
MIR217HG过度表达加剧了压力过载引起的心脏缩和纤维化,而敲击扭转了这些影响.
MIR217HG通过海绵miR-138来调节THBS1,而THBS1沉默改善了MIR217HG诱导的心脏重塑.

结论:

MIR217HG作为心脏重塑的显著诱导剂.
miR-138/THBS1通路是MIR217HG促进心脏重塑的关键机制.
通过这种途径,MIR217HG可能会导致心力衰竭的进展.

关键词:

进行心脏重塑.这是一个LncRNARNA.在MIR217HG中,MIR217HG是指MIR217HG.在THBS1中,THBS1是THBS1.这里是 miR-13838 的位置.

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