Valatas Vassilis, Filidou Eirini, Drygiannakis Ioannis, Kolios George
Laboratory of Gastroenterology, Faculty of Medicine, University of Crete, Heraklion (Vassilis Valatas, Ioannis Drygiannakis).
Laboratory of Pharmacology, School of Medicine, Democritus University of Thrace, Dragana, Alexandroupolis (Eirini Filidou, George Kolios), Greece.
Ann Gastroenterol. 2017;30(4):393-404. doi: 10.20524/aog.2017.0146. Epub 2017 Apr 12.
Post-inflammatory scarring is the end-result of excessive extracellular matrix (ECM) accumulation and tissue architectural destruction. It represents a failure to effectively remodel ECM and achieve proper reinstitution and healing during chronic relapsing inflammatory processes. Scarring may affect the functionality of any organ, and in the case of inflammatory bowel disease (IBD)-associated fibrosis leads to stricture formation and often surgery to remove the affected bowel. The activated myofibroblast is the final effector cell that overproduces ECM under the influence of various mediators generated by an intense interplay of classic and non-classic immune cells. This review focuses on how proinflammatory mediators from various sources produced in different stages of intestinal inflammation can form profibrotic pathways that eventually lead to tissue scarring through sustained activation of myofibroblasts.
炎症后瘢痕形成是细胞外基质（ECM）过度积聚和组织结构破坏的最终结果。它代表了在慢性复发性炎症过程中未能有效重塑ECM并实现适当的修复和愈合。瘢痕形成可能影响任何器官的功能，在炎症性肠病（IBD）相关纤维化的情况下，会导致狭窄形成，通常需要手术切除受影响的肠段。活化的肌成纤维细胞是最终效应细胞，在经典和非经典免疫细胞强烈相互作用产生的各种介质影响下，过度产生ECM。本综述重点关注肠道炎症不同阶段产生的各种来源的促炎介质如何形成促纤维化途径，最终通过肌成纤维细胞的持续活化导致组织瘢痕形成。
