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在糖尿病病中,miR-214及其主要转录物Dnm3os通过RAGE信号调节纤维化和炎症

Shinji Hagiwara^1,2,3, Jun Okabe^4,5, Mark Ziemann^1,4,5

¹JDRF Danielle Alberti Memorial Centre for Diabetes Complications, Diabetes Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.

|April 4, 2025

概括

这项研究揭示了microRNA-214 (miR-214) 和其宿主ncRNA,Dnm3os,在糖尿病病 (DKD) 中调节纤维化. MiR-214通过准RAGE信号来保护纤维化,而Dnm3os则可以促进纤维化.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

晚期糖化最终产品 (RAGE) 信号的受体在糖尿病病 (DKD) 发病过程中至关重要.
非编码RNAs (ncRNAs),包括microRNAs (miRs),与DKD进展有关,特别是纤维化.
在DKD中,RAGE信号与ncRNA调节之间的相互作用在很大程度上仍未被探索.

研究的目的:

在DKD的背景下,研究RAGE在ncRNA表达中的调节作用.
评估RAGE删除对糖尿病脏中ncRNA,miR和纤维/炎症标志物的影响.
为了阐明特定的ncRNAs和miRs在RAGE介导纤维化中的功能意义.

主要方法:

在糖尿病RAGE淘汰赛 (KO) 和野生型 (WT) 小鼠中对脏ncRNA和miR表达的比较分析.
在实验室中使用RAGE KO和WT小鼠中介质细胞 (MC) 进行研究,以检查ncRNA-RAGE相互作用.
在DKD小鼠模型中进行miR-214的体内给药,以评估治疗潜力.

主要成果:

在RAGE-/-和WT小鼠中,糖尿病诱导导致脏miR-214和Dnm3os水平升高,在RAGE-/-MC中表达更高.
在WT MC中,miR-214的过度表达减弱了纤维化和炎症性基因表达,而抑制则加剧了这些标记物.
人类DKD组织显示Dnm3os表达增加;miR-214向DIAPH1,一个RAGE调解器,而Dnm3os具有相反的效果.
在DKD小鼠模型中,服用miR-214显著改善了纤维化.

结论:

MiR-214和Dnm3os是DKD中纤维化的关键调节剂,通过RAGE-DIAPH1轴起作用.
米R-214作为负调节剂,通过向DIAPH1.1,抑制纤维化和炎症.
Dnm3os作为一种积极的调节剂,促进纤维化和炎症,突出了DKD病变的新型ncRNA介导途径.

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