Bronchial epithelium as a target for innovative treatments in asthma.
Key events
Mucin hypersecretion
In asthma, excessive mucus production is a hallmark of airway remodeling.
The review states that excessive mucus production is a defining feature of asthmatic airway remodeling, supporting mucin hypersecretion as a key event in human asthma.
Since many years we tried to therapeutically target mucus hypersecretion, but actually this option is still not achieved.
The review identifies mucus hypersecretion as a long-standing but still unmet therapeutic target in asthma, underscoring its relevance as a key event.
Airway inflammation
Airway inflammation is central in current asthma management.
The review names airway inflammation as the central target of current asthma management, supporting it as a key event in the asthma pathway.
Understanding of how the airway epithelium influences the TH2 paradigm in response to deleterious agents is improving.
The review places the airway epithelium upstream of the TH2 inflammatory paradigm triggered by deleterious agents, linking epithelial responses to airway inflammation.
Airway remodeling
Airway remodeling is observed in severe chronic airway diseases and may result from ongoing disturbance of signal transduction and epithelial renewal.
The review reports airway remodeling as an observed tissue-level change in severe chronic airway diseases such as asthma.
Disturbed epithelial signal transduction and renewal
Airway remodeling is observed in severe chronic airway diseases and may result from ongoing disturbance of signal transduction and epithelial renewal.
The review proposes ongoing disturbance of epithelial signal transduction and renewal as the process underlying airway remodeling, supporting it as a cellular-level key event.
Key-event relationships
Disturbed epithelial signal transduction and renewal leads to airway remodeling
The review proposes that airway remodeling in severe chronic airway diseases may result from ongoing disturbance of signal transduction and epithelial renewal. The paper's hedged wording ('may result from') is recorded as weak evidence support.
Airway remodeling is observed in severe chronic airway diseases and may result from ongoing disturbance of signal transduction and epithelial renewal.
The review states the causal hypothesis that ongoing disturbance of epithelial signal transduction and renewal drives airway remodeling.