Marônek Martin, Marafini Irene, Gardlík Roman, Link René, Troncone Edoardo, Monteleone Giovanni
Institute of Molecular Biomedicine, Faculty of Medicine, Comenius University in Bratislava, Bratislava, 81108, Slovakia.
Department of Systems Medicine, University of Rome "Tor Vergata", Rome, 00133, Italy.
J Inflamm Res. 2021 Mar 23;14:1029-1041. doi: 10.2147/JIR.S288280. eCollection 2021.
Inflammatory bowel diseases (IBD) are chronic inflammatory diseases of the gastrointestinal tract, encompassing two main disorders: Crohn's disease (CD) and ulcerative colitis (UC). In both these pathologies, excessive and local immune response against luminal antigens promotes a pathological process leading to various degrees of gut damage. Matrix metalloproteinases (MMPs) are a family of neutral proteases with the ability to degrade all components of extracellular matrix. In physiological conditions, MMPs are produced at very low level and generally in the latent form and are involved in the normal tissue turnover. Their function is inhibited by tissue inhibitors of metalloproteinases (TIMPs). However, in inflamed tissue of IBD patients, MMPs are produced in excess and/or the activity of TIMPs is not sufficient to block MMPs, thereby making a major contribution to the IBD-related mucosal degradation. In this review, we summarize the available evidence on the expression and role of MMPs in IBD.
炎症性肠病(IBD)是胃肠道的慢性炎症性疾病,包括两种主要病症:克罗恩病(CD)和溃疡性结肠炎(UC)。在这两种病理情况下,针对管腔抗原的过度局部免疫反应会促进导致不同程度肠道损伤的病理过程。基质金属蛋白酶(MMPs)是一类中性蛋白酶家族,具有降解细胞外基质所有成分的能力。在生理条件下,MMPs以非常低的水平产生,通常以潜伏形式存在,并参与正常的组织更新。它们的功能受到金属蛋白酶组织抑制剂(TIMPs)的抑制。然而,在IBD患者的炎症组织中,MMPs产生过多和/或TIMPs的活性不足以阻断MMPs,从而对IBD相关的黏膜降解起主要作用。在这篇综述中,我们总结了关于MMPs在IBD中的表达和作用的现有证据。