Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches

Article ID	Journal	Published Year	Pages	File Type
8536859	Pharmacology & Therapeutics	2018	74 Pages	PDF

Abstract

Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To date, therapeutic strategies to reduce mucus accumulation have focused primarily on altering the properties of the mucus itself, or have aimed to limit the production of mucus-stimulating cytokines. Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation and highlights both pre-existing and novel therapeutic strategies to combat this pathology.

Keywords

EGFR GCD ERK OVA TGF mTOR shRNA HNE mAb NICD HB-EGF SOCS HDM PI3K CCSP TNF cAMP MAPK short-hairpin RNA Cyclic adenosine monophosphate Asthma STAT Monoclonal antibody Akt Mechanical stress Human neutrophil elastase Ovalbumin epithelial to mesenchymal transition Epithelium COPD Chronic obstructive pulmonary disease transforming growth factor EMT Notch intracellular domain Monoclonal antibody therapy Therapeutic suppressor of cytokine signaling Goblet cell tumor necrosis factor phosphatidylinositol-3 kinase Cystic fibrosis Signal transducer and activator of transcription Mucus Signaling pathways Micro-RNA Mechanistic target of rapamycin club cell secretory protein protein kinase B mitogen activated protein kinase extracellular signal-regulated kinase House dust mite Epidermal growth factor receptor