Reactive oxygen species (ROS) are classically defined as partially reduced oxygen derivatives that possess strong oxidizing capabilities. The concept of chronic or prolonged ROS production is considered central to the progression of inflammatory disease.

ROS produced by phagocytic cells are involved in the host-defense response and act as both signaling molecules and mediators of inflammation. The ambient levels of ROS are important for the homeostasis of cells, whereas excessive ROS are important in killing pathogens. Excessive ROS and insufficient antioxidants lead to inflammatory tissue injury. Thus, the antioxidant machinery of the cell plays an essential role in setting up this intricate balance. While it is clear that ROS are important to the pathogenesis of inflammation and tissue injury, much remains unknown about how ROS function physiologically and how they contribute to the mechanism of inflammation and tissue injury.

The aim of this Special Issue is to provide a broad and updated overview of the involvement of oxidative stress in inflammation and tissue injury. Knowledge on the interaction between oxidative stress and inflammation, and their role in tissue injury (e.g., ischemia-reperfusion injury, the stress of hyperoxia or high-glucose, atherosclerosis, toxins, neurodegenerative and metabolic hormonal disorders, etc.) will help develop strategies in combating these pathological conditions. Original research and review articles are welcome.

Potential topics include but are not limited to the following:

• Sources and regulation of ROS in inflammation
• Molecular mechanisms of oxidative stress-mediated signaling in inflammation
• Interaction between ROS production and inflammatory responses
• Oxidative stress and tissue injury
• Roles of antioxidant therapy in inflammatory diseases and tissue injury
• New insights into the relationship between oxidative stress and the immune system