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血管壁的氧化应激。机制与药理学方面。

Oxidative stress at the vascular wall. Mechanistic and pharmacological aspects.

作者信息

Rojas Armando, Figueroa Hector, Re Lamberto, Morales Miguel A

机构信息

Escuela de Medicina, Facultad de Ciencias de la Salud, Universidad Católica del Maule, Talca, Chile.

出版信息

Arch Med Res. 2006 May;37(4):436-48. doi: 10.1016/j.arcmed.2005.11.012.

Abstract

During the process of energy production in aerobic respiration, vascular cells produce reactive oxygen species (ROS). A growing body of evidence indicates that oxidative stress refers to a condition in which cells are subjected to excessive levels of ROS. Overall vascular function is dependent upon a fine balance of oxidant and antioxidant mechanisms, which determine endothelial functions. Considerable experimental and clinical data indicate that intracellular oxidant milieu is also involved in several redox-sensitive cellular signaling pathways such as ion transport systems, protein phosphorylation, and gene expression and thus also plays important roles as modulator of vascular cell functions such as cell growth, apoptosis, migration, angiogenesis and cell adhesion. Overproduction of ROS under pathophysiologic conditions is integral in the development of cardiovascular diseases. This fact has raised an intensive search of new pharmacological approaches to improve vascular hemostasis and particularly those intended to decrease oxidative stress or augment the antioxidant defense mechanisms.

摘要

在有氧呼吸产生能量的过程中,血管细胞会产生活性氧(ROS)。越来越多的证据表明,氧化应激是指细胞受到过量ROS影响的一种状态。整体血管功能依赖于氧化剂和抗氧化机制的精细平衡,这些机制决定了内皮功能。大量实验和临床数据表明,细胞内氧化环境也参与了多种氧化还原敏感的细胞信号通路,如离子转运系统、蛋白质磷酸化和基因表达,因此在调节血管细胞功能(如细胞生长、凋亡、迁移、血管生成和细胞黏附)方面也发挥着重要作用。病理生理条件下ROS的过度产生是心血管疾病发生发展的一个重要因素。这一事实促使人们深入寻找新的药理学方法来改善血管止血,特别是那些旨在降低氧化应激或增强抗氧化防御机制的方法。

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