In homeostasis, the production of cellular reactive oxygen species (ROS) is generated endogenously during mitochondrial oxidative metabolism. Levels are controlled by an arsenal of local antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase. ROS products by normal cell metabolism are crucial to cell homeostasis maintenance, particularly for its role in immunocompetence and activation of several signal transduction pathways.

In the uncontrolled inflammatory response, ROS overwhelm the cellular antioxidant defense system, resulting in direct or indirect ROS-mediated damage of nucleic acids, proteins, and lipids. In the acute inflammatory process, high intracellular levels of ROS have been implicated in an impairment of resolution of inflammation and cellular injury, resulting in chronic inflammation. The imbalance due to excess ROS or oxidants reduces the ability of the cell to mount an effective antioxidant response and is implicated in airway and lung inflammatory diseases.

This Special Issue invites investigators to submit original research articles as well as review articles that aim to increase our knowledge about the effects of ROS imbalance and/or signalling on the development or aggravation of pulmonary diseases as well as the effects of compounds with antioxidant properties on acute or chronic lung diseases.

Potential topics include but are not limited to the following:

• ROS signalling pathways involved in resolution and/or chronicity of inflammatory response in lungs
• ROS imbalance involved in development or aggravation of lung diseases
• ROS-induced resistance to lung diseases therapy
• Effects of old and new compounds with antioxidant properties on pulmonary diseases