通过miR-3074-5p/DLL4轴调节巨细胞亡:对心血管疾病中Notch信号通路调节的影响
Lin Cong1,2, Lili Zhao2, Ying Shi2
1Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, China.
Aging
|August 21, 2024
概括
循环RNAs调节动脉样硬化中的巨细胞亡. Circ_0006476通过miR-3074-5p/DLL4影响细胞亡,影响心血管疾病中的Notch信号通路.
科学领域:
- 生物医学科学 生物医学科学
- 分子生物学分子生物学
- 心血管研究研究心血管研究
背景情况:
- 动脉样硬化 (AS) 是心血管疾病 (CVD) 的主要原因,随着人口老龄化而增加.
- 巨细胞亡是AS发展和进展的关键因素.
- 循环RNAs (circRNAs) 越来越多地被认可为它们在疾病中的作用,但它们在亡中的机制尚不清楚.
研究的目的:
- 为了研究circRNAs在尼古丁诱导的巨细胞亡中的作用.
- 阐明AS.的背景下,循环RNA调节的细胞亡背后的分子机制.
- 确定AS的潜在治疗点.
主要方法:
- 用尼古丁治疗的THP-1巨细胞的全转录组测序.
- 基因本体学 (GO) 和KEGG通路分析.
- 基因组丰富分析 (GSEA).
- 构建和验证一个具有竞争力的内源RNA (ceRNA) 网络.
- 分子生物学实验. 分子生物学实验.
主要成果:
- 尼古丁显著影响巨细胞的生理过程和相关途径.
- 诺奇信号通路被激活,在尼古丁治疗的巨细胞中增加DLL4表达.
- 确定Circ_0006476通过miR-3074-5p/DLL4轴参与了亡.
- 这条通路调节与Notch信号通路相关的致病过程.
结论:
- Circ_0006476通过在Notch信号通路中的miR-3074-5p/DLL4相互作用在巨细胞亡中发挥作用.
- 了解这些机制为治疗动脉样硬化提供了新的治疗策略的潜力.
- 对巨细胞亡途径的进一步研究可能会导致AS死亡率降低.
关键词:
DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4 DLL4缺口信号通道的信号通道.灭症 (apoptosis) 是一种死亡的过程.环_000647676 的时间在 miR-3074-5p 中使用.更多相关视频
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