首页> 美国卫生研究院文献>Mediators of Inflammation >Myeloperoxidase-Dependent LDL Modifications in Bloodstream Are Mainly Predicted by Angiotensin II Adiponectin and Myeloperoxidase Activity: A Cross-Sectional Study in Men
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Myeloperoxidase-Dependent LDL Modifications in Bloodstream Are Mainly Predicted by Angiotensin II Adiponectin and Myeloperoxidase Activity: A Cross-Sectional Study in Men

机译:血流中过氧化物酶依赖的LDL修饰主要由血管紧张素II脂联素和髓过氧化物酶活性预测:男性的横断面研究

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摘要

The present paradigm of atherogenesis proposes that low density lipoproteins (LDLs) are trapped in subendothelial space of the vascular wall where they are oxidized. Previously, we showed that oxidation is not restricted to the subendothelial location. Myeloperoxidase (MPO), an enzyme secreted by neutrophils and macrophages, can modify LDL (Mox-LDL) at the surface of endothelial cells. In addition we observed that the activation of the endothelial cells by angiotensin II amplifies this process. We suggested that induction of the NADPH oxidase complex was a major step in the oxidative process. Based on these data, we asked whether there was an independent association, in 121 patients, between NADPH oxidase modulators, such as angiotensin II, adiponectin, and levels of circulating Mox-LDL. Our observations suggest that the combination of blood angiotensin II, MPO activity, and adiponectin explains, at least partially, serum Mox-LDL levels.
机译:当前的动脉粥样硬化范例提出,低密度脂蛋白(LDL)被困在血管壁的内皮下空间被氧化。以前,我们表明氧化不限于内皮下的位置。髓过氧化物酶(MPO)是一种由中性粒细胞和巨噬细胞分泌的酶,可以修饰内皮细胞表面的LDL(Mox-LDL)。此外,我们观察到血管紧张素II对内皮细胞的激活会放大该过程。我们建议,NADPH氧化酶复合物的诱导是氧化过程中的重要一步。基于这些数据,我们询问了NADPH氧化酶调节剂(如血管紧张素II,脂联素)与循环Mox-LDL水平之间是否有独立的关联,在121位患者中。我们的观察结果表明,血液血管紧张素II,MPO活性和脂联素的结合至少部分解释了血清Mox-LDL水平。

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