Therapeutic strategies in inflammasome mediated diseases of the liver

被引:26
作者
Hoque, Rafaz [1 ,2 ]
Vodovotz, Yoram [3 ,4 ]
Mehal, Wajahat [1 ,2 ]
机构
[1] Yale Univ, Sect Digest Dis, New Haven, CT 06520 USA
[2] West Haven Vet Med Ctr, New Haven, CT 06520 USA
[3] Univ Pittsburgh, Dept Surg, McGowan Inst Regenerat Med, Pittsburgh, PA USA
[4] Univ Pittsburgh, Ctr Inflammat & Regenerat Modeling, McGowan Inst Regenerat Med, Pittsburgh, PA USA
关键词
ISCHEMIA-REPERFUSION INJURY; RECEPTOR; 4; ANTAGONIST; DOUBLE-BLIND; MATHEMATICAL-MODEL; CASPASE INHIBITOR; PHASE-III; HEPATITIS; PLACEBO; MICE; LIPOPOLYSACCHARIDE;
D O I
10.1016/j.jhep.2012.12.017
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Tissue stress and cell death result in inflammation even in the absence of pathogens. Such sterile inflammation is dependent on a cytosolic complex of proteins inside immune cells termed the inflammasome. This complex converts two groups of extracellular signals into an inflammatory response via activation of caspase-1 and secretion of IL-1 beta and IL-18. Group 1 signals are typically TOLL like receptor agonists and result in transcriptional upregulation of inflammasome components and pro-cytokines. Group 2 signals are diverse, ranging from uric acid to ATP, and lead to assembly and activation of the inflammasome complex. Inflammasome components are required for a wide range of acute and chronic pathologies, including experimental alcoholic and non-alcoholic steatohepatitis, and drug-induced liver injury. Collectively, group 1 and 2 signals, inflammasome components, and cytokine receptors provide a rich source of therapeutic targets. Many of the advances in the field have come from standard reductionist experiments. Progress in the understanding of complex human systems will, however, be dependent on novel strategies such as systems analysis, which analyze large data sets to provide new insights. Published by Elsevier B.V. on behalf of the European Association for the Study of the Liver.
引用
收藏
页码:1047 / 1052
页数:6
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