Inflammation and the metabolic syndrome:: Role of angiotensin II and oxidative stress
Inflammation and the metabolic syndrome:: Role of angiotensin II and oxidative stress
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DOI：
10.1007/s11906-006-0050-7
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发表时间：
2006-06-01
影响因子：
5.6
通讯作者：
Martinez-Maldonado, Manuel
中科院分区：
文献类型：
--
作者：
Ferder, Leon;Inserra, Felipe;Martinez-Maldonado, Manuel
体重过重、高血压和胰岛素抵抗一起被命名为代谢综合征。本文就血管紧张素II和活性氧在代谢综合征炎症反应中的作用进行综述。血管紧张素II诱导促炎基因和其他促炎物质，并增加氧化应激，可能损害内皮细胞，心肌和肾组织。核、因子-κ B和NAD（P）H氧化酶的活化是这些促炎机制中的基本步骤，其中线粒体内氧化应激可发挥关键作用。这一系列事件可能解释了为什么血管紧张素转换酶抑制剂（ACEIs）和血管紧张素II I型（ATI）受体阻滞剂（ARB）减少血管紧张素II合成对心血管疾病具有保护作用。
Excess body weight, high blood pressure, and insulin resistance together have been denominated the metabolic syndrome. In, this, review, we analyze the potential role of angiotensin II (Ang II) and reactive oxygen species in Mediating inflammation in the metabolic syndrome. Ang II induces pro-inflammatory genes and other pro-inflamatory substances and increases oxidative stress that could damage, endothelium, myocardium, and renal tissue. Activation of nuclear, factor-kappa B and NAD(P)H oxidase are fundamental steps in these pro-inflammatory mechanisms in which intramitochondrial oxidative stress could play a critical role. This sequence of events might explain why reduction in Ang II synthesis by angiotensin converting enzyme inhibitors (ACEIs) and Ang II type I (ATI) receptor blockers (ARBs) have a protective effect against cardiovascular disease.