Oxidative stress, initiated by burst production of reactive oxygen species (ROS), plays an important role in ischemia reperfusion injury by affecting cell death processes (apoptosis, necrosis, and autophagy). Apoptosis, autophagy, and the newly identified necroptosis are three major types of programmed cell death that participate in the pathogenesis of ischemia reperfusion injury, in which apoptosis and necroptosis function as pro-death signals that lead to cell death while autophagy is a predominantly cytoprotective process serving as a pro-survival function in ischemia reperfusion injury.

During ischemia reperfusion, oxidative stress, by inducing apoptosis and necroptosis on the one hand and by disrupting autophagy (imbalance of autophagosome formation and degradation) on the other hand, jointly causes mitochondrial dysfunction and further enhances oxidative stress, resulting in cell death and organ/cellular injury. Thus, reducing oxidative stress to maintain the balance among apoptosis, necroptosis, and autophagy is of particular importance in the attenuation of ischemia reperfusion injury. However, the molecular mechanism governing oxidative stress-induced apoptosis, necroptosis, and autophagy is unclear, and therapies targeting these three types of cell death in ischemia reperfusion injury are lacking.

We invite investigators to contribute original research articles as well as review articles that will stimulate continuing efforts to understand the molecular mechanism underlying oxidative stress-induced cell death (apoptosis, necroptosis, and autophagy) in ischemia reperfusion injury under normal and diseased conditions to develop strategies to treat these pathological conditions.

Potential topics include but are not limited to the following:

• Roles of apoptosis, necroptosis, and autophagy in organ (heart, lung, brain, liver, kidney, and/or intestine) ischemia reperfusion injury under normal and diseased conditions (e.g., diabetes and aging)
• The role of reactive oxygen species (ROS) in organ ischemia reperfusion injury under normal and diseased conditions and its interplay with apoptosis, necroptosis, and autophagy
• Cellular protective signalling pathways targeting cell death (apoptosis, necroptosis, and autophagy) that contribute to cellular repair during ischemia reperfusion injury and the potential interplay between these pathways
• Cardioprotection in aged and/or functionally impaired hearts
• Role of mitochondrial function in oxidative stress and inflammation-mediated remote organ injury during ischemia reperfusion
• Recent advances in preventing ischemia-reperfusion injury with a focus on oxidative stress and cell death