发病机制
紧密连接
基质金属蛋白酶
克洛丹
免疫系统
炎症性肠病
免疫学
医学
肠粘膜
封堵器
肠道疾病
蛋白水解酶
生物
癌症研究
疾病
酶
病理
细胞生物学
内科学
生物化学
作者
Sunisa Hankan,Pawin Pongkorpsakol
出处
期刊:Tissue barriers
[Taylor & Francis]
日期:2023-02-18
卷期号:12 (1): 2182117-2182117
被引量:1
标识
DOI:10.1080/21688370.2023.2182117
摘要
Intestinal tight junction disruption and mucosal immune dysregulation contribute to pathogenesis and progression of inflammatory bowel diseases (IBD). A proteolytic enzyme matrix metalloproteinase 7 (MMP-7), which is highly expressed in intestinal tissue, is implicated to IBD and other immune overactivation-associated diseases. In the issue of the Frontiers in Immunology, Ying Xiao and colleagues demonstrate that MMP-7-mediated claudin-7 degradation promotes IBD pathogenesis and disease progression. Therefore, inhibition of MMP-7 enzymatic activity can be a therapeutic strategy for the treatment of IBD.
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