Inflammatory bowel diseases (IBDs), including Crohn's disease (CD), ulcerative colitis (UC), and IBD-unclassified (IBD-U), are chronic inflammatory disorders of the gastrointestinal tract. Chronic inflammation in the course of IBD is an important initiating factor of fibrosis of the intestinal wall. Intestinal fibrosis is one of the most common and important complications of IBD and, due to the irreversibility of the process and the need for surgical treatment, currently poses a major clinical challenge. In this review, we presented in detail the process of intestinal wall fibrosis at the molecular, immunological, and clinical levels. We characterized the mediators, including transforming growth factor beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), and others participating in this process. We also described the type 2 epithelial-mesenchymal transition (EMT) process closely associated with chronic inflammation, leading to excessive development of connective tissue in the intestinal wall in the course of IBD.