Published online Dec 26, 2010. doi: 10.4330/wjc.v2.i12.408
Revised: September 4, 2010
Accepted: September 11, 2010
Published online: December 26, 2010
Reactive oxygen species (ROS) have long been proposed to be mediators of experimental cardiovascular pathology. There is also a wealth of data indicating that ROS are involved in clinical cardiovascular pathology. However, multiple clinical studies have shown little benefit from anti-oxidant treatments, whereas nearly all experimental studies have shown a marked effect of anti-oxidant therapy. One reason for this discrepancy is that ROS are produced through multiple different mechanisms of which some are clinically beneficial; thus, in a defined experimental system where predominately pathological ROS are generated does not mimic a clinical setting where there are likely to be multiple ROS generating systems producing beneficial and pathological ROS. Simple inhibition of ROS would not be expected to have the same result in these two situations; ergo, it is important to understand the molecular mechanism underlying the production of ROS so that clinical treatments can be tailored to target the pathological production of ROS. One such example of this in cardiovascular biology is tissue specific inflammation-mediated ROS generation. This and the following series of articles discuss the current understanding of the role of ROS in cardiovascular disease, specifically focusing on the molecular mechanisms of ROS generation and the actions of ROS within the cardiovascular system. Although there are still many areas with regard to the effects of ROS in the cardiovascular system that are not completely understood, there is a wealth of data suggesting that blocking pathological ROS production is likely to have beneficial clinical effects compared to traditional anti-oxidants.