Inflammasomes in pancreatic physiology and disease

被引:52
作者
Hoque, Rafaz [1 ]
Mehal, Wajahat Z. [1 ,2 ]
机构
[1] Yale Univ, Sch Med, Sect Digest Dis, New Haven, CT 06520 USA
[2] Dept Vet Affairs Connecticut Healthcare, Sect Digest Dis, West Haven, CT USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2015年 / 308卷 / 08期
基金
美国国家卫生研究院;
关键词
G protein-coupled receptor 109a; G protein-coupled receptor 81; mitochondrial oxidation; NACHT; LRR; and PYD domains-containing protein 3; TUMOR-NECROSIS-FACTOR; TOLL-LIKE RECEPTOR; HIGH-FAT-DIET; STERILE INFLAMMATORY RESPONSE; ACINAR-CELL NECROSIS; IL-1; RECEPTOR; REDUCES LIVER; KAPPA-B; ACTIVATION; ACID;
D O I
10.1152/ajpgi.00388.2014
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
In this review we summarize the role of inflammasomes in pancreatic physiology and disease with a focus on acute pancreatitis where much recent progress has been made. New findings have identified inducers of and cell specificity of inflammasome component expression in the pancreas, the contribution of inflammasome-regulated effectors to pancreatitis, and metabolic regulation of inflammasome activation, which are strong determinants of injury in pancreatitis. New areas of pancreatic biology will be highlighted in the context of our evolving understanding of gut microbiome-and injury-induced inflammasome priming, pyroptosis, and innate immune-mediated regulation of cell metabolism.
引用
收藏
页码:G643 / G651
页数:9
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