Crohn's disease (CD) is a chronic inflammatory disease of the gastrointestinal tract that leads to substantial suffering for millions of patients. In some patients, the chronic inflammation leads to remodelling of the extracellular matrix and fibrosis. Fibrosis, in combination with expansion of smooth muscle layers, leaves the bowel segment narrowed and stiff resulting in strictures, which often require urgent medical intervention. Although stricture development is associated with inflammation in the affected segment, anti‐inflammatory therapies fall far short of treating strictures. At best, current therapies might allow some patients to avoid surgery in a shorter perspective and no anti‐fibrotic therapy is yet available. This likely relates to our poor understanding of the mechanism underlying stricture development. Chronic inflammation is a prerequisite, but progression to strictures involves changes in fibroblasts, myofibroblasts and smooth muscle cells in a poorly understood interplay with immune cells and environmental cues. Much of the experimental evidence available is from animal models, cell lines or non‐strictured patient tissue. Accordingly, these limitations create the basis for many previously published reviews covering the topic. Although this information has contributed to the understanding of fibrotic mechanisms in general, in the end, data must be validated in strictured tissue from patients. As stricture formation is a serious complication of CD, we endeavoured to summarize findings exclusively performed using strictured tissue from patients. Here, we give an update of the mechanism driving this serious complication in patients, and how the strictured tissue differs from adjacent unaffected tissue and controls.

中文翻译：

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克罗恩病的纤维化和狭窄形成机制

克罗恩氏病（CD）是胃肠道的一种慢性炎症性疾病，导致数百万患者遭受重创。在某些患者中，慢性炎症导致细胞外基质重塑和纤维化。纤维化与平滑肌层的扩张相结合，会使肠段变窄和变硬，导致狭窄，这通常需要紧急医疗干预。尽管狭窄的发展与患病部位的炎症有关，但抗炎疗法远远不足于狭窄的治疗。最好的情况是，目前的疗法可能会使一些患者在较短的时间内避免手术，并且尚无抗纤维化疗法。这可能与我们对狭窄发展的潜在机制了解不足有关。慢性炎症是先决条件，但发展为狭窄涉及成纤维细胞，成肌纤维细胞和平滑肌细胞的变化，而这种变化与免疫细胞和环境提示的相互作用尚不清楚。现有的许多实验证据来自动物模型，细胞系或非狭窄的患者组织。因此，这些局限性为许多以前发表的有关该主题的评论奠定了基础。尽管此信息总体上有助于理解纤维化机制，但最终必须在患者的狭窄组织中验证数据。由于狭窄形成是CD的严重并发症，因此我们努力总结仅使用来自患者的狭窄组织进行的发现。在这里，我们提供了驱动这种严重并发症的机制的更新，