FIGURE 1.

Oxidative stress created by excessive generation of mitochondrial reactive oxygen species (ROS) plays well-recognized roles in the development of an array of cardiovascular disorders leading to sudden cardiac death. ROS production can be amplified through the process of ROS-induced ROS release (RIRR), causing cellular dysfunction and death, directly creating a pro-arrhythmic substrate (solid arrows). In a relatively more indirect manner, ROS production can increase the risk of lethal arrhythmias by promoting adverse remodeling of various pathways in the diabetic heart (dashed arrows) (Wilson et al., 2018). Similarly, ROS production can contribute to the progression of atherosclerosis and myocardial infarction as well as to heart failure-associated cardiac remodeling, increasing the susceptibility of the heart to arrhythmias that can result in sudden cardiac death.