TY - JOUR
T1 - The role of emtu in mucosae remodeling: Focus on a new model to study chronic inflammatory lung diseases
AU - Burgio, Stefano
AU - Pitruzzella, Alessandro
AU - Intili, Giorgia
AU - Fucarino, Alberto Giuseppe
AU - Pitruzzella, Alessandro
AU - Fucarino, Alberto
AU - Nigro, Chiara Lo
AU - Nigro, Chiara Lo
AU - Marchese, Roberto
AU - Saguto, Dario
AU - Modica, Domenico Michele
PY - 2020
Y1 - 2020
N2 - In recent years, part of the scientific community has focused its attention on the involvement of the epithelial-mesenchymal trophic unit (EMTU) in mucosa remodeling, monitoring its role in chronic inflammatory lung diseases. The term EMTU is used to describe the anatomic and functional relationship between the attenuated fibroblast sheath and epithelial tissue, i.e. the signaling between epithelial cells and the underlying fibroblasts, which are in close indirect physical contact with the former. These interactions are important for many airway functions, such as differentiation during lung growth, repair of damaged tissue and regulation of inflammatory response. Several studies have indicated a key role for the EMTU in the processes that influence mucosae remodelling. These processes can be observed in different pathologies, such as asthma or chronic obstructive pulmonary disease (COPD). This review focuses on the primary role of the EMTU in mucosa remodeling, aiming to give a contribution to an issue that, if deepened may lead to more efficient treatments for the handling of chronic respiratory diseases. The close correlation between the reactivation of the EMTU in adult age and the onset of chronic diseases of the respiratory system is now widely accepted by the scientific community. It is therefore of fundamental importance to enhance our knowledge on its reactivation and the processes that lead to tissue remodeling. Pinpointing the key molecular pathways would provide new therapeutic targets for limiting the remodeling processes typical of subjects suffering from different types of airway pathologies.
AB - In recent years, part of the scientific community has focused its attention on the involvement of the epithelial-mesenchymal trophic unit (EMTU) in mucosa remodeling, monitoring its role in chronic inflammatory lung diseases. The term EMTU is used to describe the anatomic and functional relationship between the attenuated fibroblast sheath and epithelial tissue, i.e. the signaling between epithelial cells and the underlying fibroblasts, which are in close indirect physical contact with the former. These interactions are important for many airway functions, such as differentiation during lung growth, repair of damaged tissue and regulation of inflammatory response. Several studies have indicated a key role for the EMTU in the processes that influence mucosae remodelling. These processes can be observed in different pathologies, such as asthma or chronic obstructive pulmonary disease (COPD). This review focuses on the primary role of the EMTU in mucosa remodeling, aiming to give a contribution to an issue that, if deepened may lead to more efficient treatments for the handling of chronic respiratory diseases. The close correlation between the reactivation of the EMTU in adult age and the onset of chronic diseases of the respiratory system is now widely accepted by the scientific community. It is therefore of fundamental importance to enhance our knowledge on its reactivation and the processes that lead to tissue remodeling. Pinpointing the key molecular pathways would provide new therapeutic targets for limiting the remodeling processes typical of subjects suffering from different types of airway pathologies.
KW - Chronic respiratory diseases
KW - Epithelial tissue
KW - Epithelial-mesenchymal trophic unit
KW - Mucosae remodelling
KW - Chronic respiratory diseases
KW - Epithelial tissue
KW - Epithelial-mesenchymal trophic unit
KW - Mucosae remodelling
UR - http://hdl.handle.net/10447/403512
M3 - Article
VL - 15
SP - 4
EP - 10
JO - EuroMediterranean Biomedical Journal
JF - EuroMediterranean Biomedical Journal
SN - 2279-7165
ER -