间充质干细胞
急性胰腺炎
医学
趋化因子
肿瘤坏死因子α
斯科普斯
免疫学
癌症研究
炎症
内科学
病理
生物
梅德林
生物化学
作者
Il Sang Shin,Chang‐Hwan Park,Jong Ho Moon,Jun Kyu Lee,Min Jae Yang,Don Haeng Lee
出处
期刊:Gastroenterology
[Elsevier BV]
日期:2023-02-18
卷期号:164 (7): 1317-1320.e2
被引量:3
标识
DOI:10.1053/j.gastro.2023.02.009
摘要
The pathophysiologic mechanism of acute pancreatitis (AP) involves autodigestion after activation of digestive enzymes. After the activation of acinar cells, chemokines promote the aggregation of helper T cells and macrophages. 1 Pandol S.J. et al. Gastroenterology. 2007; 132: 1127-1151 Abstract Full Text Full Text PDF PubMed Scopus (494) Google Scholar This induces the production of inflammatory cytokines (interleukin [IL]-1β, IL-4, IL-5, IL-6, IL-10, interferon-γ, and tumor necrosis factor-α), thereby triggering inflammatory cascades and leading to systemic inflammatory response syndrome, multiorgan failure, and, in some cases, death. 1 Pandol S.J. et al. Gastroenterology. 2007; 132: 1127-1151 Abstract Full Text Full Text PDF PubMed Scopus (494) Google Scholar ,2 Malmstrøm M.L. et al. Pancreas. 2012; 41: 271-277 Crossref PubMed Scopus (117) Google Scholar
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