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在高脂肪饮食诱导的超脂血症中识别潜在的致病性肝超增强剂监管网络

Yingying Hu¹, Run Xu¹, Jing Feng¹

¹Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China and Key Laboratory of Cardiovascular Medicine Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, China.

The Journal of nutritional biochemistry

|January 19, 2024

概括

超级增强剂 (SE) 调节参与高脂血症 (HLP) 的基因. 这项研究确定了HPL特定的SE和监管网络,揭示了HPL和心血管疾病的潜在治疗点.

科学领域:

基因组学就是基因组学.
分子生物学分子生物学
代谢障碍代谢障碍代谢障碍

背景情况:

超脂血症 (HLP) 是心血管疾病的主要危险因素.
超级增强剂 (SE) 对于细胞身份和疾病进展中的基因调节至关重要.
在HPL开发中SE的作用仍然在很大程度上未被探索.

研究的目的:

调查SEs在超脂血症的发病过程中的作用.
识别特定于HLP的SE及其相关的监管网络.
为了发现HPL的潜在治疗点.

主要方法:

综合分析H3K27acChIP-seq和RNA测序数据从低脂肪和高脂肪饮食下的小鼠肝脏组织.
使用超级增强剂的排名排序算法识别和描述超级增强剂 (SE).
基因本体学 (GO) 和KEGG通路丰富分析,蛋白质-蛋白质相互作用网络构建和转录因子预测.

主要成果:

在低脂肪和高脂肪饮食组分别发现了1877个和1847个SE.
SE抑制剂JQ1逆转了饮食诱导的脂质积累,证实了SE参与脂质代谢.
确定了278种高脂肪饮食特异性SE (HSEs),主要与脂质代谢途径有关.
确定了四个枢纽基因 (Cd36,Pex11a,Ech1,Cidec),并建立了一个HSE特定的监管网络.

结论:

超级增强剂在超脂血症的发病过程中起着重要作用.
已识别的高质量企业和监管网络为HLP机制提供了新的见解.
这项研究突出了潜在的治疗点,如Cidec和Cd36,用于HPL治疗.

关键词:

有高脂肪的饮食.超脂血症是因为高脂血症脂质新陈代谢脂质新陈代谢肝脏肝脏肝脏肝脏超级增强剂超级增强剂

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