Table 1.

Main signaling pathways involved in controlling the initiation and progression of epithelial to mesenchymal transition (EMT) during neural polypogenesis. The formation of the nasal polyp is supported by a marked tissue remodeling process induced by various inflammatory mediators and modulation of intra-cellular signaling pathways. The resulting EMT can be inhibited by signal transduction inhibitors, leading to the loss of epithelial gene expression and the simultaneous acquisition of the molecular component properties typical of mesenchymal cells.

PATHWAYS	CRSwNP	Inhibitors of EMT	Ref.
TGF-β1	downregulated	HDAC1/2, TSA Chemical chaperones, PBA, PPB TGF-β1 miR-21 Glucocorticoids	[35,36,38,39]
SMAD3 and HIF-1α	upregulated	HIF-1α inhibitors 2ME2, 17-AAG	[40]
AGE/RAGE/ERK	upregulated	p38, MEK, ERK inhibitors	[41]
MEK1/2-ERK1/2	upregulated	MEK, ERK inhibitors	[42,43,44]
WNT/ β-catenin/GSK	upregulated	Wnt inhibitors IWP2 oxide 1,8-cineol inhibitor GSK-3	[45,46,47,48]
PPAR-γ	upregulated	agonist PPAR-γ Rosiglitazone	[49]