期刊
ACTA PHYSIOLOGICA
卷 205, 期 1, 页码 26-40出版社
WILEY
DOI: 10.1111/j.1748-1716.2012.02391.x
关键词
beta adrenergic; cardiac contractility; endothelin; reactive oxygen species; signal transduction
类别
资金
- Hungarian Scientific Research Fund [K69118]
- Academy of Finland
- Sigrid Juselius Foundation
- Finnish Foundation for Cardiovascular Research
- Foundation for the Development of Interventional Cardiology
Increased production of reactive oxygen species (ROS) has been linked to the pathogenesis of congestive heart failure. However, emerging evidence suggests the involvement of ROS in the regulation of various physiological cellular processes in the myocardium. In this review, we summarize the latest findings regarding the role of ROS in the acute regulation of cardiac contractility. We discuss ROS-dependent modulation of the inotropic responses to G protein-coupled receptor agonists (e.g. beta-adrenergic receptor agonists and endothelin-1), the potential cellular sources of ROS (e.g. NAD(P)H oxidases and mitochondria) and the proposed end-targets and signalling pathways by which ROS affect contractility. Accumulating new data supports the fundamental role of endogenously generated ROS to regulate cardiac function under physiological conditions.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据