Reactive Oxygen-Induced Cardiac Intracellular Pathways During Ischemia and Reperfusion

Reactive oxygen species (ROS) are involved in cardiovascular diseases and, in particular, in myocardial ischemia and reperfusion. Although the restoration of blood flow is essential for salvation of ischemic heart, reperfusion elicits itself additional tissue damages. This condition has been defined as myocardial-reperfusion injury. ROS have been firstly studied for their deleterious role during reperfusion, including protein oxidation, DNA strand breaks, lipids peroxydation or opening of mitochondrial permeability transition pore, that are all potentially harmful for the cell survival. Indeed, ROS are massively generated at the onset of reperfusion, contributing to the post-ischemic oxidative stress and mitochondrial dysfunction and ultimately leading to cardiomyocyte death. Animal studies using antioxidant treatments have shown beneficial and encouraging effects in myocardial ischemia-reperfusion. However, univocal interpretations of the results from clinical trials remain uncertain and controversial. Recently, another role of ROS had been highlighted. Multiple evidences had shown that ROS act as essential mediators of cardioprotection, mainly during pre- and post-conditioning. Thus, free radicals in myocardial ischemia reperfusion injury may be not considered just as detrimental but also as protective molecules. This review summarizes recent findings about this dual role of ROS in myocardial ischemia-reperfusion injury.