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通过调节miR-3113-5p/CTGF和miR-3473d/FN1轴,LncRNA CFRL会加剧心脏纤维化

Yue Cui¹, Bozhong Shi¹, Zijie Zhou¹

¹Department of Cardiothoracic Surgery, Shanghai Children's Medical Center Affiliated to Shanghai Jiao Tong University School of Medicine, 1678 Dongfang Road, Shanghai 200127, China.

|November 13, 2023

概括

一种新发现的长非编码RNA,心脏纤维化相关的lncRNA (CFRL),通过调节纤维细胞活动来促进心脏纤维化. 在体内抑制CFRL减轻了纤维化和改善了心脏功能,这表明CFRL是治疗点.

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
非编码RNA研究研究

背景情况:

心脏纤维化是心力衰竭发展的关键因素.
长非编码RNAs (lncRNAs) 的失调与心脏病有关.
开发有效的心脏纤维化治疗方法仍然具有挑战性.

研究的目的:

为了识别和描述与心脏纤维化有关的新型 lncRNA.
阐明CFRL在心脏纤维化中的作用背后的分子机制.
评估针对心脏纤维化和心力衰竭的CFRL的治疗潜力.

主要方法:

使用了体外 (细胞培养) 和体内 (小鼠模型) 两种方法.
心脏纤维化模型中的量化CFRL表达.
研究了CFRL与微RNA (miR-3113-5p,miR-3473d) 和基因 (CTGF,FN1) 的相互作用.
评估了CFRL沉默对心脏纤维化和左心室功能的影响.

主要成果:

鉴定并命名为lncRNA NONMMUT067673.2作为与心脏纤维化相关的lncRNA (CFRL).
在心脏纤维化模型中,CFRL表达显著上调.
在体外,CFRL通过海绵miR-3113-5p和miR-3473d促进心脏纤维细胞的增殖和迁移,提高CTGF和FN1.
在体内,沉默CFRL减弱心脏纤维化和改善心脏功能.

结论:

CFRL在心脏纤维化病原发生过程中起着至关重要的作用.
通过调节miR-3113-5p/miR-3473d-CTGF/FN1轴,CFRL促进心脏纤维化.
向CFRL代表了对心脏纤维化和心力衰竭的潜在多目标治疗策略.

关键词:

心血管医学心血管医学人类遗传学人类遗传学分子医学是分子医学.

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