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氧化应激和活性氧在心血管疾病中的作用不断变化的概念。

Evolving concepts of oxidative stress and reactive oxygen species in cardiovascular disease.

机构信息

Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, 55 Lake Avenue N., S3-851, Worcester, MA 01655, USA.

出版信息

Curr Atheroscler Rep. 2012 Oct;14(5):476-83. doi: 10.1007/s11883-012-0266-8.

Abstract

Cardiovascular disease (CVD) continues to be a substantial health-care burden, despite recent treatment advances. Oxidative stress has long been regarded as a key pathophysiological mediator that ultimately leads to CVD including atherosclerosis, hypertension and heart failure. Over the past decade, emerging evidence has shifted our understanding of reactive oxygen species (ROS) from its harmful role to being signaling molecules. Here, we reviewed recent advances in our understanding of ROS that mediate the complex process of CVDs, with a focus on major ROS signaling and sources such as mitochondria and Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidases.

摘要

心血管疾病 (CVD) 尽管最近有了治疗进展,但仍然是一个巨大的医疗保健负担。氧化应激一直被认为是关键的病理生理介质,最终导致 CVD,包括动脉粥样硬化、高血压和心力衰竭。在过去的十年中,新出现的证据改变了我们对活性氧 (ROS) 的理解,使其从有害角色转变为信号分子。在这里,我们回顾了近年来对 ROS 的理解的最新进展,这些进展介导了 CVD 的复杂过程,重点介绍了主要的 ROS 信号和来源,如线粒体和烟酰胺腺嘌呤二核苷酸磷酸 (NADPH) 氧化酶。

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