Figure 1.

Chronic inflammation in Crohn’s disease results in fibrostenosis of the intestinal wall. Increased pro-inflammatory and pro-fibrotic stimuli activate submucosal myofibroblasts which differentiate into smooth muscle cells. Activated myofibroblasts, and fibroblasts differentiated through the epithelial to mesenchymal transition (EMT) or the endothelial to mesenchymal transition (EndoMT), produce excess of extracellular matrix (ECM). As a result, smooth muscle cell hyperplasia and hypertrophy take place, along with increased deposition of ECM, thus producing an overall thickening of the intestinal wall with narrowing of the lumen in the fibrostenotic state.