TABLE 3.

Molecular mechanisms implicated in the downregulation of type-2 EMT in IBD samples, and in vivo and in vitro IBD related models. The symbol “/” indicates treatment. Bone morphogenic protein-7 (BMP7); Dextran sodium sulfate (DSS); Glycogen synthase kinase (GSK); Intestinal epithelial cell (IEC); Peroxisome proliferator-activated receptor (PPARγ); Silent information regulator 1 (SIRT1); Transforming growth factor (TGF); Trinitrobenzene sulfonic acid (TNBS); Vitamin D (VD); Vitamin D receptor (VDR).

Protein	Type of study		EMT	Molecular mechanism in EMT	References
BMP7	In vivo	TNBS VillinCre; R26Rosa-lox-STOP-lox-LacZ mice (trace IECs)	↓	BMP7 is an inhibitor of TGFβ	Flier et al. (2010)
GSK3β/PPARγ	In vivo	DSS/GW9662 (PPARγ inhibitor) DSS/GED-0507-34 Levo (PPARγ agonist)	↓	GSK3β activate PPARγ signaling	Di Gregorio et al. (2017)
SIRT1	In vitro In vivo	IEC6/TGFβ TNBS SIRT1−/−	↓	Blocks TGFβ through SMAD4 and KDM4-DBC1axis	Simic et al. (2013), Chen et al. (2021)
VDR	In vitro In vivo Human	HT29, CCDA18Co cells/VD TNBS VDR−/−CD: ↓VDR	↓	Epithelial mitochondria-mediated EMT	Yu et al. (2021)