<p>Intestinal fibrosis is a common and severe complication in the progression of inflammatory bowel disease (IBD). Its pathological essence lies in the excessive synthesis and abnormal deposition of extracellular matrix (ECM) components within the intestinal tissue, leading to structural remodeling and dysfunction of the intestinal wall. As the disease progresses, fibrosis is primarily characterized by the pathological thickening of the muscularis propria, which subsequently triggers irreversible structural damage, such as intestinal strictures, severely impacting patients’ quality of life and prognosis. Currently, clinical interventions for intestinal fibrosis are relatively limited, mainly relying on pharmacotherapy and surgical resection. However, existing drugs primarily focus on controlling the inflammatory response in IBD rather than directly targeting the fibrotic process, making it difficult to effectively block or reverse ECM accumulation. Although surgery can temporarily relieve obstruction, it is associated with a high postoperative recurrence rate and fails to fundamentally intervene in the pathological mechanisms of fibrosis. Therefore, a deeper understanding of the mechanisms underlying the initiation and progression of intestinal fibrosis is of great significance for developing specific anti-fibrotic therapeutic strategies and improving long-term patient outcomes. This review aims to systematically summarize the cellular and molecular mechanisms of intestinal fibrosis, with a focus on the roles of fibroblast activation, epithelial–mesenchymal transition, and immune microenvironment regulation in the fibrotic process. The goal is to provide a theoretical basis and novel research insights for the subsequent development of targeted drugs and the optimization of clinical treatment strategies.</p>