在压力过载下由雄激素介导的右心室不适应性重塑的基于蛋白质和代谢的机制
Jing Zhang1, Xiaohan Qin1, Yuhan Qin1
1Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
概括
雄激素通过增加氧化应激和损害能量供应,可能通过PDGFRB-STAT3通路恶化男性的右心室重塑. 这条路径的路径.
科学领域:
- 心血管生物学 心血管生物学
- 内分泌学 在内分泌学.
- 蛋白质组学和代谢组学
背景情况:
- 右心室 (RV) 不适应性重塑在男性中比女性更严重.
- 雄激素参与其中,但驱动这种性别差异的潜在机制是未知的.
研究的目的:
- 为了研究素加剧RV不适应性重塑的分子机制.
- 为了确定参与性别特定RV改造的关键途径.
主要方法:
- 在接受肺动脉带纹 (PAB) 的雄性和割大鼠中,蛋白质组和代谢组.
- 在用替代的老鼠中验证,途径抑制剂研究,以及对RV重塑患者样本的分析.
- 使用二次光谱匹配进行代谢物验证.
主要成果:
- 雄性PAB大鼠比割的PAB大鼠显示出更大的VR缩和纤维化.
- 奥米克斯的分析显示,男性的氧化应激增加和脂肪酸代谢下调.
- 血小板衍生生长因子 (PDGF) 途径,特别是PDGFRB-STAT3信号,被激活并与VR重塑联系在一起,抑制剂在男性中逆转了重塑.
结论:
- 雄激素可能会通过增加氧化应激和能量赤字恶化RV不适应性重塑.
- 激活PDGFRB-STAT3信号通路是一种潜在的机制,可以调解雄激素诱导的RV重塑.
- 准这种途径为男性的RV重塑提供了潜在的治疗策略.
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