Disruption of the airway epithelial barrier plays a major role in the initiation and progression of chronic lung disease. Exposure to environmental allergens or respiratory viruses triggers adaptive injury repair responses in the airway. These insults trigger epithelial-mesenchymal plasticity, a multi-step genomic reprogramming process producing activation of epithelial-mesenchymal transition (EMT) and simultaneously mesenchymal-epithelial transition (MET) programs. Although epithelial plasticity facilitates organ injury repair, this cell-state transition disrupts epithelial barrier function, stimulating the release of fibroblastic growth factors, triggering metabolic adaptations, extracellular matrix (ECM) generation, tissue remodeling, and affecting innate mucosal immune responses. Through changes in secreted growth factors, ECM remodeling and release of matricellular proteins, fibroblast-to-myofibroblast conversion.
This field is rapidly advancing with the applications of next-generation sequencing, protein and metabolomic profiling, and assays that probe chromatin occupancy and state. The goal of this thematic issue is to provide a forum for the exchange of current developments in the complex adaptations of the airways to environmental injury. Papers that address the following questions are highly encouraged.
Topics could include, but not be limited to:
• Mechanisms of epithelial plasticity in the airway produced by allergens, viruses, or oxidative (reactive oxygen or nitrogen) stress.
• Roles and consequences of epithelial plasticity in allergic or fibrotic airway diseases, and potential therapies.
• Relationship of genomic reprogramming in epithelial stress response on metabolic adaptations, extracellular matrix (ECM) remodeling, or myofibroblast expansion.
We are seeking original research articles or relevant up-to-date review articles.
Disruption of the airway epithelial barrier plays a major role in the initiation and progression of chronic lung disease. Exposure to environmental allergens or respiratory viruses triggers adaptive injury repair responses in the airway. These insults trigger epithelial-mesenchymal plasticity, a multi-step genomic reprogramming process producing activation of epithelial-mesenchymal transition (EMT) and simultaneously mesenchymal-epithelial transition (MET) programs. Although epithelial plasticity facilitates organ injury repair, this cell-state transition disrupts epithelial barrier function, stimulating the release of fibroblastic growth factors, triggering metabolic adaptations, extracellular matrix (ECM) generation, tissue remodeling, and affecting innate mucosal immune responses. Through changes in secreted growth factors, ECM remodeling and release of matricellular proteins, fibroblast-to-myofibroblast conversion.
This field is rapidly advancing with the applications of next-generation sequencing, protein and metabolomic profiling, and assays that probe chromatin occupancy and state. The goal of this thematic issue is to provide a forum for the exchange of current developments in the complex adaptations of the airways to environmental injury. Papers that address the following questions are highly encouraged.
Topics could include, but not be limited to:
• Mechanisms of epithelial plasticity in the airway produced by allergens, viruses, or oxidative (reactive oxygen or nitrogen) stress.
• Roles and consequences of epithelial plasticity in allergic or fibrotic airway diseases, and potential therapies.
• Relationship of genomic reprogramming in epithelial stress response on metabolic adaptations, extracellular matrix (ECM) remodeling, or myofibroblast expansion.
We are seeking original research articles or relevant up-to-date review articles.