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高血压中的氧化应激与血管损伤:血管紧张素II的作用

Oxidative Stress and Vascular Damage in Hypertension: Role of Angiotensin II.

作者信息

Virdis Agostino, Duranti Emiliano, Taddei Stefano

机构信息

Department of Internal Medicine, University of Pisa, 56100 Pisa, Italy.

出版信息

Int J Hypertens. 2011;2011:916310. doi: 10.4061/2011/916310. Epub 2011 May 26.

Abstract

Reactive oxygen species are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. In healthy conditions, ROS are produced in a controlled manner at low concentrations and function as signaling molecules regulating vascular contraction-relaxation and cell growth. Physiologically, the rate of ROS generation is counterbalanced by the rate of elimination. In hypertension, an enhanced ROS generation occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. In the present paper, major angiotensin II-induced vascular ROS generation within the vasculature, and relative sources, will be discussed. Recent development of signalling pathways whereby angiotensin II-driven vascular ROS induce and accelerate functional and structural vascular injury will be also considered.

摘要

活性氧是氧的衍生物,在血管生物学中发挥着积极作用。这些化合物在血管壁内、内皮细胞和血管平滑肌细胞水平以及外膜成纤维细胞中产生。在健康状态下,活性氧以可控方式在低浓度下产生,并作为调节血管收缩 - 舒张和细胞生长的信号分子发挥作用。生理上,活性氧的产生速率与消除速率相平衡。在高血压中,活性氧的产生增强,而内源性抗氧化机制无法平衡这种增强,从而导致氧化应激状态。在本文中,将讨论血管紧张素 II 诱导的血管内主要活性氧产生及其相关来源。还将考虑血管紧张素 II 驱动的血管活性氧诱导和加速血管功能和结构损伤的信号通路的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/362f/3124711/424f112d1355/IJHT2011-916310.001.jpg

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