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Assessing Murine Resistance Artery Function Using Pressure Myography
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在高血压中,UBR1促进了性取决于ACE2的ubiquitination
Mona Elgazzaz1,2,3,4, Navya Lakkappa1,2,3, Clara Berdasco1,2,3
1Cardiovascular Center of Excellence (M.E., N.L., C.B., U.P.M., A.N., L.R., A.M., A.S., J.J.G., S.S., J.X., X.Y., C.M.F., E.L.), New Orleans, LA.
Hypertension (Dallas, Tex. : 1979)
|November 27, 2024
概括
乌比奎丁蛋白联酶E3成分N-recognin (UBR1) 向抗高血压酶血管素转化酶2 (ACE2) 降解,导致高血压. 准UBR1可能会恢复ACE2功能并治疗高血压.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 高血压研究 高血压研究
背景情况:
- ангиотензин II (Ang-II) 损害了 ангиотензин转化酶 2 (ACE2) 的功能,促进了高血压.
- 已知很少有ACE2无处不在的合作伙伴,它们在高血压中的作用尚不清楚.
研究的目的:
- 在高血压小鼠中识别ACE2无处不在的合作伙伴.
- 调查确定合作伙伴在维持高血压中的作用.
主要方法:
- 蛋白质组学和生物信息学以确定ACE2无处不在的合作伙伴.
- 基于细胞的UBR1-ACE2相互作用的验证.
- 在高血压的雄性小鼠中,体内UBR1被淘汰.
主要成果:
- UBR1被确定为一种促进ACE2无化和降解的E3酶.
- 在高血压小鼠和人类中,UBR1表达升高,与降低的ACE2有关.
- 在雄性小鼠中,UBR1倒置恢复了ACE2水平,并暂时降低了血压.
- 丸激素,而不是雌激素,对性别进行特定的调节UBR1.1.
结论:
- UBR1是一种新型的E3泛素酶,向高血压中的ACE2.
- UBR1和Nedd4-2可能会协同无处不在地激活ACE2.
- 向UBR1和Nedd4-2可以恢复高血压中的ACE2活性.
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