Suppression of oxidative stress in the endothelium and vascular wall
Suppression of oxidative stress in the endothelium and vascular wall
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DOI：
10.1080/10623320490482600
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发表时间：
2004-03-01
影响因子：
--
通讯作者：
Dusting, GJ
中科院分区：
文献类型：
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作者：
Jiang, F;Drummond, GR;Dusting, GJ
越来越多的证据表明，氧化应激，即活性氧和氮物质的过度产生，是许多形式的心血管疾病的基础。动脉壁中氧化应激的主要来源是NADPH氧化酶。血管细胞（包括内皮细胞）中的这种酶复合物在生化结构和功能上与吞噬性白细胞中的酶复合物不同。含黄素的关键催化亚基Nox 1和Nox 4不存在于白细胞中，但在血管细胞中高度表达，并在血管重塑中上调，如在高血压和动脉粥样硬化中发现的。这提供了开发“血管特异性”NADPH氧化酶抑制剂的机会，其不损害由活性氧和氮分子进行的基本生理信号传导和吞噬功能。尽管许多常规抗氧化剂未能显著影响心血管疾病的结果，但阻断血管系统中氧化应激源的NADPH氧化酶的靶向抑制剂更有可能预防导致中风和心脏病发作的血管功能恶化。
There is growing evidence that oxidative stress, meaning an excessive production of reactive oxygen and nitrogen species, underlies many forms of cardiovascular disease. The major source of oxidative stress in the artery wall is an NADPH oxidase. This enzyme complex in vascular cells, including endothelium, differs from that in phagocytic leucocytes in both biochemical structure and functions. The crucial flavin-containing catalytic subunits Nox1 and Nox4 are not present in leucocytes, but are highly expressed in vascular cells and upregulated in vascular remodeling, such as that found in hypertension and atherosclerosis. This offers the opportunity to develop "vascular specific" NADPH oxidase inhibitors that do not compromise the essential physiological signaling and phagocytic function carried out by reactive oxygen and nitrogen molecules. Although many conventional antioxidants; fail to significantly affect outcomes in cardiovascular disease, targeted inhibitors of NADPH oxidase that block the source of oxidative stress in the vasculature are more likely to prevent the deterioration of vascular function that leads to stroke and heart attack.