首页> 外文期刊>Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease >Arginase-II Induces Vascular Smooth Muscle Cell Senescence and Apoptosis Through p66Shc and p53 Independently of Its l-Arginine Ureahydrolase Activity: Implications for Atherosclerotic Plaque Vulnerability
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Arginase-II Induces Vascular Smooth Muscle Cell Senescence and Apoptosis Through p66Shc and p53 Independently of Its l-Arginine Ureahydrolase Activity: Implications for Atherosclerotic Plaque Vulnerability

机译:精氨酸酶II诱导血管平滑肌细胞衰老和凋亡通过p66Shc和p53独立于其1-精氨酸尿素水解酶活性:对动脉粥样硬化斑块易感性的影响。

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Background Vascular smooth muscle cell (VSMC) senescence and apoptosis are involved in atherosclerotic plaque vulnerability. Arginase-II (Arg-II) has been shown to promote vascular dysfunction and plaque vulnerability phenotypes in mice through uncoupling of endothelial nitric oxide synthase and activation of macrophage inflammation. The function of Arg-II in VSMCs with respect to plaque vulnerability is unknown. This study investigated the functions of Arg-II in VSMCs linking to plaque vulnerability.
机译:背景血管平滑肌细胞(VSMC)的衰老和凋亡与动脉粥样硬化斑块易损性有关。精氨酸酶II(Arg-II)已被证明可以通过解耦内皮一氧化氮合酶和激活巨噬细胞炎症来促进小鼠血管功能障碍和斑块易损性表型。关于斑块易损性,Arg-II在VSMC中的功能尚不清楚。这项研究调查了Arg-II在VSMC中与斑块易损性相关的功能。

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