In homeostasis, the production of cellular reactive oxygen species (ROS) is generated endogenously during mitochondrial oxidative metabolism. An arsenal of local antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase controls ROS levels. 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 that aim to increase our knowledge about the oxidative stress-associated mechanisms, signaling pathways, and corresponding therapeutics in the pathogenesis and treatment of acute or chronic lung diseases.

Potential topics include but are not limited to the following:

• ROS signaling pathway as central component of maintenance of homeostasis
• Role of oxidative stress in resolution of inflammation
• Role of oxidative stress in acute or chronic inflammation
• Effects of old and newest compounds on lung inflammatory diseases