About this Research Topic
The airway barrier is a dynamic entity which is constantly exposed to external stimuli that could pave the way for lung dysfunction. The exposure to noxious stimuli such as pathogens, cigarette smoke or particulate matter alters lung barrier in that pathological events can occur. In particular, loss of compartmentalization, hyperproliferation and inflammation can underlie noxious stimuli-induced pulmonary diseases. To date, the exposure to external dangerous stimuli can also lead to the release of endogenous alarmins, which altogether can affect the respiratory function.
The main goal of this Research Topic is to highlight molecular and cellular mechanisms involved in pulmonary endothelial and epithelial impairment responsible for lung barrier dysfunction.
Therefore, we propose the following goals to be reached:
1. Define external noxious stimuli and endogenous alarmins that can alter lung barrier by altering the physiological role of the endothelial and epithelial pulmonary cells;
2. Identify mechanisms that can alter the physiological role of the endothelial and epithelial pulmonary cells;
3. Highlight potential cross-talks among the proposed mechanisms that underlie external stimuli or endogenous alarmins-induced lung pathologies (i.e. chronic obstructive pulmonary disease (COPD), idiopathic fibrosis, lung cancer, etc.).
Highlight molecular and cellular mechanisms that underlie lung barrier dysfunction with an ensuing alteration of the endothelial and epithelial integrity represents the main goal of this Research Topic.
The main focuses are as following:
- Role of the immune system (circulating and resident immune cells, inflammatory mediators, inflammasome complex, complement system) in regulating pulmonary endothelial and epithelial integrity during physiological conditions and airway diseases (e.g. acute lung injury, COPD, pulmonary fibrosis, oedema, pulmonary hypertension, cancer);
- Lipidic mediators (bio-, phospo-, sphingo-lipids) as lung barrier integrity protectors/destroyers;
- Cell-cell junctions, epithelial to mesenchymal transition and alveolar/capillary permeability alterations after exogenous (e.g. infectious agents, allergens, cigarette smoke, air pollutants, drugs) and/or endogenous stimuli;
- Platelets and coagulation system involvement;
- Cellular metabolism dysfunction, mitochondrial dysfunction, oxidative stress, ER stress, cell death;
- Gene alterations;
- Mechanisms of tissue repair and vascular remodeling.
We encourage Original Research articles and Reviews, as well as Perspective studies.
The main goal of this Research Topic is to highlight molecular and cellular mechanisms involved in pulmonary endothelial and epithelial impairment responsible for lung barrier dysfunction.
Therefore, we propose the following goals to be reached:
1. Define external noxious stimuli and endogenous alarmins that can alter lung barrier by altering the physiological role of the endothelial and epithelial pulmonary cells;
2. Identify mechanisms that can alter the physiological role of the endothelial and epithelial pulmonary cells;
3. Highlight potential cross-talks among the proposed mechanisms that underlie external stimuli or endogenous alarmins-induced lung pathologies (i.e. chronic obstructive pulmonary disease (COPD), idiopathic fibrosis, lung cancer, etc.).
Highlight molecular and cellular mechanisms that underlie lung barrier dysfunction with an ensuing alteration of the endothelial and epithelial integrity represents the main goal of this Research Topic.
The main focuses are as following:
- Role of the immune system (circulating and resident immune cells, inflammatory mediators, inflammasome complex, complement system) in regulating pulmonary endothelial and epithelial integrity during physiological conditions and airway diseases (e.g. acute lung injury, COPD, pulmonary fibrosis, oedema, pulmonary hypertension, cancer);
- Lipidic mediators (bio-, phospo-, sphingo-lipids) as lung barrier integrity protectors/destroyers;
- Cell-cell junctions, epithelial to mesenchymal transition and alveolar/capillary permeability alterations after exogenous (e.g. infectious agents, allergens, cigarette smoke, air pollutants, drugs) and/or endogenous stimuli;
- Platelets and coagulation system involvement;
- Cellular metabolism dysfunction, mitochondrial dysfunction, oxidative stress, ER stress, cell death;
- Gene alterations;
- Mechanisms of tissue repair and vascular remodeling.
We encourage Original Research articles and Reviews, as well as Perspective studies.
Keywords: Lung barrier integrity/alteration, acute and chronic lung injury, lung epithelial cells, pulmonary endothelial cells
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.
