期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 109, 期 -, 页码 61-74出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2017.02.012
关键词
eNOS; NADPH oxidase; Heart failure; Superoxide; Hydrogen peroxide; Glutaredoxin; S-glutathionylation
资金
- National Health and Medical Research Council
- Heart Foundation of Australia Fellowship [APP 1062262]
- Heart Research Australia
Rapid and coordinated release of a variety of reactive oxygen species (ROS) such as superoxide (O2(.-)), hydrogen peroxide (H2O2) and peroxynitrite, in specific microdomains, play a crucial role in cell signalling in the cardiovascular system. These reactions are mediated by reversible and functional modifications of a wide variety of key proteins. Dysregulation of this oxidative signalling occurs in almost all forms of cardiovascular disease (CVD), including at the very early phases. Despite the heavily publicized failure of antioxidants to improve CVD progression, pharmacotherapies such as those targeting the renin-angiotensin system, or statins, exert at least part of their large clinical benefit via modulating cellular redox signalling. Over 250 proteins, including receptors, ion channels and pumps, and signalling proteins are found in the caveolae. An increasing proportion of these are being recognized as redox regulated-proteins, that reside in the immediate vicinity of the two major cellular sources of ROS, nicotinamide adenine dinucleotide phosphate oxidase (Nox) and uncoupled endothelial nitric oxide synthase (eNOS). This review focuses on what is known about redox signalling within the caveolae, as well as endogenous protective mechanisms utilized by the cell, and new approaches to targeting dysregulated redox signalling in the caveolae as a therapeutic strategy in CVD.
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