自噬
炎症
巨噬细胞
炎症性肠病
医学
免疫系统
免疫学
发病机制
疾病
平衡
癌症研究
生物
细胞凋亡
病理
体外
内科学
遗传学
作者
Er-jin Wang,Chuanbin Yang,Zheng‐Yu Ren,Ying Zheng,Richard D. Ye,Chris Soon Heng Tan,Yitao Wang,Jiahong Lu
出处
期刊:Burns & Trauma
[Oxford University Press]
日期:2023-01-01
卷期号:11
被引量:13
标识
DOI:10.1093/burnst/tkad004
摘要
Abstract Inflammatory bowel disease (IBD) is a chronic, non-specific, recurrent inflammatory disease, majorly affecting the gastrointestinal tract. Due to its unclear pathogenesis, the current therapeutic strategy for IBD is focused on symptoms alleviation. Autophagy is a lysosome-mediated catabolic process for maintaining cellular homeostasis. Genome-wide association studies and subsequent functional studies have highlighted the critical role of autophagy in IBD via a number of mechanisms, including modulating macrophage function. Macrophages are the gatekeepers of intestinal immune homeostasis, especially involved in regulating inflammation remission and tissue repair. Interestingly, many autophagic proteins and IBD-related genes have been revealed to regulate macrophage function, suggesting that macrophage autophagy is a potentially important process implicated in IBD regulation. Here, we have summarized current understanding of macrophage autophagy function in pathogen and apoptotic cell clearance, inflammation remission and tissue repair regulation in IBD, and discuss how this knowledge can be used as a strategy for IBD treatment.
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