Reactive oxygen species-induced reactive oxygen species release in vascular signaling and disease

Reactive oxygen species (ROS) derived from both nicotinamide adenine dinucleotide phosphate oxidase (NOX) and mitochondria play a critical role in many physiological and pathological processes. However, how highly diffusible ROS produced from different sources can coordinate to drive angiogenesis and other responses is poorly understood. Recently, the cross-talk between NOX and mitochondria, termed “ROS-induced ROS release (RIRR)” has been proposed as a mechanism for ROS amplification and localized ROS production. NOX-derived ROS increase mitochondrial ROS while mitochondrial ROS stimulate NOX activation. This RIRR mechanism may represent a feed-forward vicious cycle of ROS production, which can be targeted under conditions of oxidative stress or enhanced in physiological condition. In this chapter, we will summarize the recent knowledge regarding the RIRR involved in vascular signaling and disease especially focusing on angiogenesis.