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LncRNA CHKB-DT 降低调节通过 ALDH2 增强扩展性心肌病

Xiang Nie¹, Jiahui Fan¹, Beibei Dai^1,2

¹Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College (X.N., J.F., B.D., Z.W., H.L., C.C., D.W.W.), Huazhong University of Science and Technology, Wuhan, China.

Circulation research

|February 1, 2024

概括

长非编码RNACHKB-DT在扩张性心肌病 (DCM) 中是下调的. 恢复CHKB-DT可以改善心脏功能和能量代谢,这表明它是DCM的潜在治疗标.

科学领域:

心血管生物学心血管生物学
分子遗传学分子遗传学
非编码RNA研究研究

背景情况:

扩张性心肌病 (DCM) 与心脏长非编码RNA (lncRNA) 档案的改变有关.
在人类DCM心脏中,lncRNA CHKB-DT (胆激酶β分离转录) 显著下调.

研究的目的:

阐明CHKB-DT在DCM病变发生中的功能作用.
调查CHKB-DT作为DCM的潜在治疗标.

主要方法:

定量逆转录-聚合酶连锁反应和现场杂交用于lncRNA表达分析.
由CRISPR/Cas9生成的CHKB-DT淘汰赛小鼠模型和基因相关病毒介导的基因传递.
评估心肌细胞收缩性,线粒体功能 (海马XF试验) 和ATP生产.
机理学研究包括定量蛋白质组学,核糖体分析和RNA-蛋白相互作用试验 (例如,RNA拉下,光酶试验).

主要成果:

在DCM患者和心力衰竭小鼠模型中证实了CHKB-DT下调.
在心肌细胞中CHKB-DT异性淘汰导致心脏扩张,功能障碍和收缩能力降低.
在CHKB-DT淘汰赛模型中观察到线粒体功能障碍,ATP生产减少和心脏能量代谢受损.
CHKB-DT直接针对ALDH2mRNA,影响其稳定性和下游4-HNE生产. 恢复ALDH2在淘汰赛小鼠中改善了心脏缺陷.

结论:

CHKB-DT在DCM中显著下调,在维持心脏功能和能量代谢方面起着至关重要的作用.
CHKB-DT充当与能量代谢相关的lncRNA,是DCM的一个有前途的治疗点.

关键词:

长非编码的RNA,长非编码的RNA 心肌病,扩张心肌病,扩张心肌病.胆激酶是一种胆激酶.能量代谢能量代谢心脏衰竭是因为心脏衰竭.

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相关概念视频

lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...