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长非编码RNA AK144717通过调节HMGB1的细胞分布和随后的DNA损伤反应来加剧病态心脏缩

Tianyu Wu¹, Yao Lu², Yue Yu³

¹Section of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Guangzhou Road 300, Nanjing, 210029, PR China.

Cellular and molecular life sciences : CMLS

|October 12, 2024

概括

一种新的长非编码RNA,AK144717,通过与HMGB1相互作用和调节DNA损伤反应 (DDR) 来加剧心脏缩. 向AK144717为病态心脏生长提供了一个潜在的治疗策略.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

心脏缩涉及DNA损伤响应 (DDR) 信号传递,由突变的太阳系外接质 (ATM) 中介.
氧化应激会导致DNA损伤,激活DDR并促进病态心肌细胞的生长.

研究的目的:

研究长非编码RNAs (lncRNAs) 在心脏缩和DDR中的作用.
确定与病态心脏生长相关的新型 lncRNAs.

主要方法:

在模拟和横向大动脉收缩 (TAC) 鼠标模型中对心室 lncRNAs 的微阵列分析.
功能性研究涉及对lncRNA AK144717和高流动性组盒1 (HMGB1) 的沉默.
评估ATM-DDR信号传输,HMGB1乙化和HMGB1-SIRT1相互作用.

主要成果:

一种新的lncRNA,AK144717,被确定并发现在TAC或 ангиотензинII (AngII) 诱导的心脏缩期间被上调.
沉默AK144717表现出类似于ATM抑制的抗缩作用,并抑制了ATM-DDR信号传输.
AK144717的作用与其与HMGB1的相互作用有关,防止HMGB1-SIRT1结合,并促进HMGB1乙化和细胞突移.

结论:

AK144717通过与HMGB1相互作用和调节DDR通路,在病态心脏缩中发挥重要作用.
AK144717代表了治疗病态心脏生长的潜在治疗标.

关键词:

心脏过度缩小的情况.对DNA损伤的反应反应在HMGB1乙化过程中,在 LncRNAs 中.

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