Department of Gastroenterology, Ghent University, Ghent, Belgium.
VIB Center for Inflammation Research, Ghent, Belgium.
J Dig Dis. 2020 Jun;21(6):319-325. doi: 10.1111/1751-2980.12882. Epub 2020 Jun 28.
Intestinal fibrosis is one of the biggest challenges in the therapeutic management of inflammatory bowel diseases (IBD). Patients with Crohn's disease, in particular, suffer from fibrotic complications, which are manifested by the clinical stenosis of the bowel. Although fibrosis is caused by recurrent episodes of inflammation and wound healing, current therapies for IBD do not seem to reduce the incidence of stenosis, suggesting that inflammation-independent mechanisms also contribute to intestinal fibrogenesis. The lack of anti-fibrotic therapies for IBD and the huge burden this complication places on patients has prompted us to redirect inflammation research toward understanding the mechanisms that drive gut fibrosis. Based on data from other fibroproliferative diseases, metabolic modifications are increasingly recognized as pathogenic processes that may generate new therapeutic opportunities. These metabolic alterations result from a switch in the cellular metabolism of activated fibroblasts, which are the key mediator cells of fibrosis. Here, we review the metabolic changes associated with fibrotic disease and summarize the evidence of a metabolic shift during intestinal fibrosis.
肠纤维化是炎症性肠病（IBD）治疗管理中最大的挑战之一。患有克罗恩病的患者尤其会遭受纤维性并发症的困扰，其表现为肠道的临床狭窄。尽管纤维化是由炎症反复发作和伤口愈合引起的，但目前针对 IBD 的治疗方法似乎并不能降低狭窄的发生率，这表明炎症独立的机制也可能导致肠道纤维化。缺乏针对 IBD 的抗纤维化治疗方法，以及这种并发症给患者带来的巨大负担，促使我们将炎症研究的方向转向理解驱动肠道纤维化的机制。基于其他纤维增生性疾病的数据，代谢修饰越来越被认为是可能产生新治疗机会的致病过程。这些代谢改变源于活化的成纤维细胞的细胞代谢发生转变，而这些成纤维细胞是纤维化的关键中介细胞。在这里，我们回顾了与纤维性疾病相关的代谢变化，并总结了在肠道纤维化过程中代谢转变的证据。
