Mechanisms of Oxidative Cellular Injury: Redox Imbalance, Signaling Pathways and Implications for Human Lung Diseases

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Background

Extensive research in recent years has suggested that low levels of reactive oxygen species (ROS) are essential for redox signaling, and normal physiological health, while supraphysiologic levels can lead to disrupted signaling, and cellular injury. Many human diseases are associated with or exacerbated by oxidative stress and novel approaches to mitigate oxidative stress are needed for prevention and/or treatment. Roles for redox mechanisms have been defined in the pathophysiology of pulmonary diseases such as asthma, bronchopulmonary dysplasia (BPD), acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and pulmonary hypertension, making redox-related processes a logical target for prevention and therapeutic development. Furthermore, in Covid-19 pathogenesis, the lung is the main target organ, making this area of respiratory pharmacology very challenging thus supporting the need for extensive research. In particular, with the new variants being discovered, the need to develop novel drugs to protect the lungs from SARS-Cov-2, and understand the mechanisms of action are urgent. Because inflammation (e.g., cytokine storm) precedes severe lung disease, research on the mechanisms of inflammatory cascades associated with severe lung disease is needed as well. Finally, the airway microbiome and the gut-lung axis in the modulation of lung diseases is an underdeveloped area and new discoveries may contribute valuable new information. Ultimately, the research in these areas will lead to novel preventative and therapeutic approaches to combat human respiratory diseases.

The problem areas we would like to address are asthma, bronchopulmonary dysplasia (BPD), acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), pulmonary hypertension, and Covid-19-mediated lung diseases. The major goal will be to address the role of reactive oxygen species (ROS) and oxidative stress in each of the above-mentioned diseases. We would also like to determine the mechanisms by which environmental exposures might modulate oxidative stress, and also cause dysbiosis of the airway microbiome and the gut-lung axis. Research on the mechanisms of Covid-19 pathogenesis, specifically focusing on lung diseases is also one of the goals. Research articles (original and reviews) focusing on the above areas will help advance our understanding of the molecular mechanisms of lung diseases, which will in turn lead to novel preventive and therapeutic approaches against lung diseases.

We invite authors to contribute original research articles as well as review articles that will illustrate and stimulate the rapid advances that are taking place in the field of preventative/therapeutic development to address redox mechanisms and human lung diseases. We are particularly interested in manuscripts describing studies targeting redox signaling pathways for the treatment of pulmonary diseases using animal or in vitro models.

We welcome submissions related but not limited to the following mechanisms for targeting redox, for the prevention and treatment of:

• asthma, BPD, ARDS, pulmonary hypertension

• ROS and redox signaling in lung diseases

• Age-related pulmonary disease and redox stress

• Covid-19 pathogenesis focused on respiratory system

• Role of airway microbiome, including gut-lung axis on lung diseases

• Effect of environmental exposures on lung injury

• Biochemical mechanisms (including role of cytochrome P450, phase II enzymes, Ah receptor, nrf2) in lung diseases

Keywords: Oxidative stress; reactive oxygen species; redox imbalance; molecular signaling, lung diseases

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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