Table 1.

Potential genetic factors of IBD-associated fibrosis

Related genes	Disease entity	Mechanism	Reference
NOD2	CD and UC	Apoptosis and activates NF-κB, induce interleukin 1-beta	[19–23]
TLR4	CD	Initiating innate immune responses	[19]
IL23R	CD and UC	Activation of Th17 lymphocytes	[27,28]
IL12B	CD	Activation of Th17 lymphocytes	[25]
JAK2	CD	Activation of Th17 lymphocytes	[29]
CX3CR1	CD	Leukocyte chemotaxis and adhesion	[30]
STAT3	CD and UC	Innate immune mechanisms	[25,26]
ATG16L1	CD	Autophagocytosis	[31]
IRGM	CD	Autophagocytosis	[25]
FUT2	CD	Affects the composition of the gut microbiota	[32]
TGF-β	CD	Initiation of inflammation	[33,34]
MMP3	CD and UC	Mediate degradation of components of the extracellular matrix	[35]
MAGI1	CD	Disruption of epithelial barrier via abrnormality of tight junction of intestinal epithelial cells	[36]

IBD, inflammatory bowel disease; NOD2, nucleotide-binding oligomerization domain-containing protein 2; CD, Crohn disease; UC, ulcerative colitis; NF-κB, nuclear factor κB; TLR4, Toll-like receptors 4; IL23R, interleukin-23 receptor; IL12B, interleukin-12 subunit beta; JAK2, Janus kinases 2; CX3CR1, C-X3-C motif chemokine receptor 1; STAT3, signal transducers and activators of the transcription 3; ATG16L1, autophagy-related 16-like 1; IRGM, immunity-related GTPase family M protein; FUT2, fucosyltransferase 2; TGF-β, transforming growth factor beta; MMP-3, matrix metalloproteinase-3; MAGI1, membrane-associated guanylate kinase inverted 1.