Novel roles for nox oxidases in cardiac arrhythmia and oxidized glutathione export in endothelial function.
Novel roles for nox oxidases in cardiac arrhythmia and oxidized glutathione export in endothelial function.
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Nox 氧化酶在心律失常中的新作用和氧化型谷胱甘肽输出在内皮功能中的新作用。
DOI：
10.1161/01.res.0000186804.96482.78
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发表时间：
2005
影响因子：
20.1
通讯作者：
Gupte,SachinA
中科院分区：
文献类型：
--
作者：
Wolin,MichaelS;Gupte,SachinA
This issue of Circulation Research contains two articles in the area of oxidant regulation that have major implications for their novel roles in mechanisms that contribute to cardiovascular disease processes in humans. An article by Kim et al1 reports data showing that human cardiac myocytes isolated from right atrial appendages express NAD (P) H oxidase (Nox)-2, and that these myocytes and homogenates of the atria from patients with atrial fibrillation (AF) have increased levels of Nox-derived superoxide generation that appear to originate from increased Nox oxidase activation. Homogenates of atria from the AF patients also show evidence of nitric oxide synthase (NOS) becoming a source of superoxide generation, which is thought to originate from an uncoupling of the ability of this enzyme to efficiently synthesize NO. The article by Mueller et al2 reports a new important role for multidrug resistance protein-1 (MRP-1) in controlling oxidant regulation in human and animal endothelium by exporting oxidized glutathione (GSSG). In their study, this group demonstrates how the expression of this protein functions to remove increased GSSG in hypertensive rats and endothelial cells exposed to oscillatory shear stress. Interestingly, the inhibition of MRP-1 appears to restore endothelial function in the hypertensive rats and prevent shear-induced apoptosis in these models apparently through preserving endothelial cell glutathione levels. Both of these articles have major new implications for the understanding and therapeutic targeting of human disease processes.
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10.1242/dev.40.1.229
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期刊：
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