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局部过氧酸盐损害了内皮暂时受体潜在化物4通道,并提高了肥胖患者的血压

Matteo Ottolini^1,2, Kwangseok Hong¹, Eric L Cope¹

¹Robert M. Berne Cardiovascular Research Center (M.O., K.H., E.L.C., Z.D., L.J.D., C.M., N.Y.N., S.R.J., B.E.I., S.K.S.).

|February 4, 2020

概括

肥胖会通过降低内皮TRPV4通道活性来降低血压调节,这是与过氧酸盐损害AKAP150相关的问题. 在肥胖患者中抑制过氧酸盐恢复正常的血压和血管扩张.

科学领域:

心血管生理学
内皮细胞生物学
高血压研究

背景情况:

内皮依赖的血管扩张对于血压调节至关重要,并且在肥胖引起的高血压中受损.
暂时受体潜在化物4 (TRPV4) 通道是内皮信号和血管扩张的关键.
AKAP150蛋白增强TRPV4通道活性,但其在与肥胖相关的高血压中的作用尚不清楚.

研究的目的:

研究内皮细胞AKAP150-TRPV4信号在肥胖患者血压调节中的作用.
确定过氧酸盐是否会损害肥胖患者的信号通路.
评估过氧的治疗潜力.

主要方法:

使用内皮特异性淘汰和高脂肪饮食诱导的肥胖小鼠模型.
评估过氧化对AKAP150-TRPV4信号和血管扩张的影响.
对人类动脉进行检查以评估临床相关性.

主要成果:

肥胖症降低了TRPV4通道的降血作用.
在肥胖小鼠中,氧化矛盾地减弱了TRPV4活性和血管扩张.
在Cys36中氧化了AKAP150, 损害了AKAP150-TRPV4信号传递和血管扩张.
降低过氧酸盐水平可以挽救肥胖症的信号,血管扩张和血压.
在肥胖患者的动脉中观察到类似的过氧酸盐依赖性损伤.

结论:

损坏的内皮TRPV4通道有助于肥胖引起的高血压.
过氧酸盐对AKAP150造成的损伤是关键机制.
抑制过氧酸盐可以恢复内皮功能并使肥胖的血压正常.

关键词:

信号传递细胞内膜高血压离子通道氧化过氧化物

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