Intestinal fibrosis

Intestinal fibrosis describes the excessive accumulation of extracellular matrix proteins—mainly collagen—within the intestinal wall following chronic inflammation or injury. This maladaptive wound-healing response leads to thickening and stiffening of affected segments, resulting in luminal narrowing (“strictures”) that can cause obstruction requiring surgical intervention. The pathogenesis involves persistent activation of mesenchymal cells (fibroblasts/myofibroblasts), immune cell infiltration perpetuating inflammation, dysregulated cytokine signaling (notably TGF‑β), epithelial-mesenchymal transition processes, and altered ECM turnover regulated by enzymes such as matrix metalloproteinases and their inhibitors. While several molecules within these pathways represent potential therapeutic targets—including TGF‑β receptors—the term “intestinal fibrosis” itself does not denote any one druggable entity but rather an end-stage manifestation common in IBD patients who do not respond adequately to anti-inflammatory therapy alone. “Intestinal fibrosis” should be classified as a pathological process rather than an individual molecular target suitable for direct pharmacological intervention.

Other names

Fibrosis of the intestineIntestinal stricturing (in context)Bowel wall scarring

Mechanisms for drugs targeting intestinal fibrosis focus on: - Inhibition of TGF‑β/Smad signaling pathway - Modulation of ECM turnover via MMPs/TIMPs balance. These mechanisms aim to reduce fibroblast activation and ECM accumulation.