LAUSR

Ischemia and reperfusion (I/R) cause a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, opening of mitochondrial permeability transition pores (mPTPs) and promotion of cell death (apoptosis or necrosis). PKC-δ and PKC-ε, belonging to a family of serine/threonine kinases, have been demonstrated to play important roles during I/R injury in cardiovascular diseases. However, the cardioprotective mechanisms of PKC-δ and PKC-ε in I/R injury have not been elaborated until now. This article discusses the roles of PKC-δ and PKC-ε during myocardial I/R in redox regulation (redox signaling and oxidative stress), cell death (apoptosis and necrosis), Ca2+ overload, and mitochondrial dysfunction.