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肺高血压通过NOX1/4-TRPM2信号通路诱导冠状动脉中的血清激素过度反应和代谢重编程

Yan-Zhen Huang¹, Ji-Chun Wu², Gui-Feng Lu¹

¹Key Laboratory of Fujian Province Universities on Ion Channel and Signal Transduction in Cardiovascular Diseases, Department of Physiology and Pathophysiology, School of Basic Medical Sciences (Y.-Z.H., G.-F.L., H.-B.L., S.-M.L., Y.-C.L., L.-X.G., M.-J.L., D.-C.L.), Fujian Medical University, Fuzhou, China.

Hypertension (Dallas, Tex. : 1979)

|January 4, 2024

概括

肺高血压 (PH) 激活了NOX-TRPM2通路,增加了血清素的反应性,并破坏了冠状动脉中的线粒体. 这一途径有助于PH的冠状动脉重塑.

科学领域:

心血管生物学心血管生物学
肺高血压研究肺高血压研究
血管生物学血管生物学

背景情况:

肺高血压 (PH) 与冠状动脉 (CA) 疾病有关,但机制尚不清楚.
血清素,活性氧物种和信号传递都与PH和CA疾病有关.
NADPH氧化酶 (NOXs) 和TRPM2通道是PH和CA疾病之间相互作用的关键参与者.

研究的目的:

研究NOX-TRPM2途径在PH中冠状动脉重塑中的作用.
为了阐明PH和CA疾病之间的机械联系.

主要方法:

使用了由慢性缺氧和单克罗他林诱导的PH的老鼠模型.
分析了CA血管反应,基因表达,新陈代谢和线粒体功能.
在CA光滑肌细胞中使用NOX1/4和TRPM2抑制剂和siRNA.

主要成果:

PH大鼠显示出显著的CA重塑和血激素过度反应.
NOX1 / 4介导的活性氧物种和TRPM2介导的流量推动了血清素的高反应性.
NOX1/4-TRPM2通路促进了CA光滑肌肉细胞的增殖,迁移,亡和代谢变化.
这一途径参与了线粒体功能障碍,包括DNA损伤和改变处理.
在体内 Knockdown 的NOX1/4 降低了PH严重性和CA重塑.

结论:

在CA光滑肌细胞中,PH激活NOX1/4-TRPM2通路,增加血清的反应性,并导致代谢和线粒体功能障碍.
NOX1/4-TRPM2信号通路是CA重塑和PH中CA疾病发展的关键因素.

关键词:

在NADPH氧化酶中,NADPH具有氧化作用.冠状动脉疾病是一种冠状动脉疾病.高血压,肺部高血压,肺部高血压.代谢重编程是指代谢重编程.线粒体中的线粒体.

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