Intestinal fibrosis is characterised by the accumulation of extracellular matrix (ECM) within the intestinal walls (Lenti and Di Sabatino 2019). Indeed, fibrogenesis is a self-limiting physiological process triggered by harmful stimuli aimed at restoring damaged tissue to its original state. However, in conditions of chronic inflammation, such as that of inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), this process takes a pathological turn, resulting in irreversible structural and functional damage to the intestine. While, to some extent, the occurrence of fibrosis is important to limit the spread of inflammation, in more advance phases, it has a detrimental effect on bowel functions, eventually leading to the need for surgery (Lenti and Di Sabatino 2019).

While inflammation triggers fibrosis, it has become increasingly evident that this process can progress independently and be self-sustaining, although the exact causes are unknown (Rieder et al., 2016a, Rieder et al., 2016b). Fibrosis involves a complex interplay of molecules and cells, making it a heterogeneous and intricate condition that poses challenges for effective treatment. Recent discoveries have significantly expanded our understanding of the pathogenesis of intestinal fibrosis, unveiling new therapeutic targets that hold promise for addressing this unmet medical need (Yoo et al., 2020, D'Alessio et al., 2022).

Therefore, in this review, we will summarize the current knowledge about intestinal fibrosis, starting from the pathogenesis of this condition, the clinical aspects, and the potential therapeutic targets.