乌比基特异性蛋白酶38促进由压力过载引起的炎症性心房动
Zheng Xiao1,2,3, Yucheng Pan1,2,3, Bin Kong1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan 430060, Hubei, China.
概括
乌比基特异性蛋白酶38 (USP38) 通过加剧炎症促进心房动 (AF). 抑制USP38改善了AF脆弱性,并在压力过载模型中减少了心房重塑.
科学领域:
- 心血管生物学 心血管生物学
- 分子心脏病学分子心脏病学
- 心房动病理生理学
背景情况:
- 前庭动 (AF) 是由结构和电气重塑驱动的.
- 在心脏功能中,乌比基特异蛋白酶38 (USP38) 的作用尚不清楚.
研究的目的:
- 调查USP38对压力过载引起的AF的影响.
- 阐明USP38在AF中的作用背后的分子机制.
主要方法:
- 使用心脏特异性的USP38淘汰和转基因小鼠.
- 在大动脉带化 (AB) 后评估了AF脆弱性,心房结构和分子标志物.
- 分析了USP38与核因子-kappa B (NF-κB) 和其下游目标的相互作用.
主要成果:
- USP38淘汰赛小鼠在AB后表现出降低AF易感性,心房重量,纤维化和改善处理.
- USP38过度表达恶化了AF和心房重塑.
- USP38二基因化NF-κB,增加p-NF-κB,NOD类受体蛋白3 (NLRP3) 和炎症性细胞因子.
结论:
- USP38促进压力过载引起的AF.
- USP38针对NF-κB/NLRP3炎症通路,以驱动不良的心脏重塑和AF.
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