Cardiovascular disease development is significantly influenced by the effects of reactive species (RS). By virtue of their controlled production, regulation, and reactive nature, RS play important roles in the modulation of cellular signaling, growth, and death in the vasculature. Concentration gradients are important in determining the effects of RS. Low to moderate concentrations of RS act as mediators in signaling cascades and gene regulation, whereas high levels of RS cause cellular damage and death. Because a dual redox regulation state seems to exist in several signaling cascades, e.g., RS often induce upstream initiating events, whereas downstream events are reliant on reductive processes, alterations in cellular redox states influence the activation/inactivation of signaling events and transcription factors. In this review, the relationships between RS, specific signal transduction pathways, and aspects of cell-cycle control are discussed.