Fig. 1.

Cellular and molecular components implicated in intestinal fibrosis. Intestinal strictures are characterized by extracellular matrix (ECM) accumulation, intestinal muscularis propria thickening, and mesenteric fat wrapping. Myofibroblasts, the major source of ECM production, can originate from various types of mesenchymal cells. Immune cells contribute to persistent myofibroblasts proliferation and activation by secreting abundant cytokines. In addition, inflammatory-independent factors including gut microbiota, ECM interaction, creeping fat and metabolic reprogramming are involved in fibrosis formation.

EMT, epithelial-mesenchymal transition; EndMT, endothelial-mesenchymal transition; FFAs, free fatty acids; FNs, fibronectins; HA, hyaluronan.