细胞内膜网膜与压力相关的基因表达通过诱导亡导致扩张性心肌病的进展
Jinhao Chen1,2, Xu Yang1,2, Weiwen Li1,2
1Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.
Frontiers in genetics
|May 3, 2024
概括
细胞内膜网膜应激 (ERS) 诱导的亡在扩张性心肌病 (DCM) 中起作用. 四个关键基因 (MX1,MYH6,TESPA1,THBS4) 在DCM中失调,为疾病机制提供了新的见解.
科学领域:
- 分子生物学分子生物学
- 心血管研究研究心血管研究
- 细胞应激反应的应激反应
背景情况:
- 细胞内膜网膜应激 (ERS) 诱导的亡与扩张性心肌病 (DCM) 的病原发生有关.
- 在DCM中形成ERS的精确分子机制尚不完全理解.
研究的目的:
- 识别和表征涉及DCM发展的ERS相关基因.
- 阐明将ERS诱导的亡与DCM病原发生联系起来的分子途径.
主要方法:
- 对差异表达基因 (DEGs) 的综合分析,加权基因共同表达网络分析 (WGCNA) 和内质网膜压力相关基因 (ERG) 的综合分析.
- 在这些数据集的交叉点识别关键基因.
- 对基因共同表达网络,竞争性内源性RNA (ceRNA) 相互作用和潜在的环境目标的分析.
主要成果:
- 在DEGs,WGCNA模块和ERG的交叉点确定了8个基因,这些基因与免疫和血管生成有关.
- 四个基因 (MX1,MYH6,TESPA1,THBS4) 特别与DCM的亡有关,它们在病毒反应,处理,炎症和瘤功能方面有着不同的作用.
- XIST被确定为影响MX1和THBS4的ceRNA网络中的关键调节者;发现BPA和VPA等环境毒素准MX1,MYH6和THBS4.
结论:
- 四个与ERS相关的基因 (MX1,MYH6,TESPA1,THBS4) 在DCM中显著失调,并与亡有关.
- 这些发现增强了对ERS诱导的亡在DCM发展中的作用的理解.
- 鉴定的基因和途径为DCM的未来治疗策略提供了潜在的目标.
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