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血管紧张素II与氧化应激

Angiotensin II and oxidative stress.

作者信息

Hitomi Hirofumi, Kiyomoto Hideyasu, Nishiyama Akira

机构信息

Department of Cardiorenal and Cerebrovascular Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.

出版信息

Curr Opin Cardiol. 2007 Jul;22(4):311-5. doi: 10.1097/HCO.0b013e3281532b53.

Abstract

PURPOSE OF REVIEW

Angiotensin II regulates vasoconstriction, homeostasis of salt and water, and cardiovascular hypertrophy and remodeling. Angiotensin II is a potent activator of NAD(P)H oxidase in the cardiovascular system, and augments production of reactive oxygen species. Numerous signaling pathways in response to angiotensin II are mediated by reactive oxygen species and oxidative stress is deeply associated with the progression of cardiovascular disease. The purpose of this review is to discuss the mechanism of reactive oxygen species formation and the pathophysiological effects of angiotensin II in the cardiovascular system.

RECENT FINDINGS

Recent studies have demonstrated novel molecular mechanisms of reactive oxygen species generation by angiotensin II and signaling pathways including cell proliferation, hypertrophy and apoptosis. In spite of these findings that strongly suggest the benefits of angiotensin II inhibition for cardiovascular disease, the clinical effects of angiotensin II-induced reactive oxygen species on the cardiovascular system are still controversial.

SUMMARY

We focus on the effects of angiotensin II-induced oxidative stress on cardiovascular function and remodeling after discussing the source of reactive oxygen species and novel signaling pathways in response to reactive oxygen species.

摘要

综述目的

血管紧张素II调节血管收缩、盐和水平衡以及心血管肥大和重塑。血管紧张素II是心血管系统中烟酰胺腺嘌呤二核苷酸磷酸(NAD(P)H)氧化酶的强效激活剂,并增加活性氧的产生。血管紧张素II引发的众多信号通路由活性氧介导,氧化应激与心血管疾病的进展密切相关。本综述旨在探讨活性氧形成的机制以及血管紧张素II在心血管系统中的病理生理作用。

最新发现

近期研究揭示了血管紧张素II产生活性氧的新分子机制以及包括细胞增殖、肥大和凋亡在内的信号通路。尽管这些发现强烈提示抑制血管紧张素II对心血管疾病有益,但血管紧张素II诱导的活性氧对心血管系统的临床影响仍存在争议。

总结

在讨论了活性氧的来源和响应活性氧的新信号通路后,我们重点关注血管紧张素II诱导的氧化应激对心血管功能和重塑的影响。

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