Summary
In this review, attempts are made to establish the role of reactive oxygen species as signaling molecules which regulate cellular and molecular basis of ischemic heart disease. Ischemia/reperrusion is a classical example for free radical signaling, because partial or mild ischemia can lead to the generation of reactive oxygen species (ROS) which simultaneously perform execution and repair of the cardiomyocytes. Execution occurs with the death signaling in which ROS play a crucial role while repair process is mediated by adaptive response in which oxygen free radicals function as typical signaling molecules through the activation of receptor tyrosine kinases, protein kinase C and MAP kinases as well as induction of redox-sensitive transcription factors and genes.