Interleukin 18 in the heart

被引：65

作者：

Wang, Meijing ^{[1
]}

Markel, Troy A. ^{[1
]}

Meldrum, Daniel R. ^{[1
,2
,3
]}

机构：

[1] Indiana Univ, Sch Med, Dept Surg, Indianapolis, IN 46202 USA

[2] Indiana Univ, Sch Med, Dept Cellular & Integrat Physiol, Indianapolis, IN USA

[3] Indiana Univ, Sch Med, Ctr Immunobiol, Indianapolis, IN USA

来源：

SHOCK | 2008年 / 30卷 / 01期

关键词：

inflammation; myocardium; ischemia; sepsis; cytokines;

D O I：

10.1097/SHK.0b013e318160f215

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

IL-18, originally termed as interferon gamma (IFN-gamma) inducing factor, is a proinflammatory cytokine that belongs to the IL-1 cytokine superfamily. IL-18 plays an important role in immune, infectious, and inflammatory diseases due to its induction of IFN-gamma. However, accumulated evidence has demonstrated that other effects of IL-18 are independent of IFN-gamma. Here, we reviewed the current literatures regarding the role of IL-18 in the heart and cardiovascular system. Infiltrated neutrophils, resident macrophages, endothelial cells, smooth muscle cells, and cardiomyocytes in the heart are able to produce IL-18 in response to injury. IL-18 is produced as a biologically inactive precursor (pro-IL-18) that is activated by caspase 1 (the IL-1 beta converting enzyme). Elevated IL-1 8 levels have been observed in cardiac tissue and circulation after myocardial I/R and sepsis. The possible cellular and molecular mechanisms concerning IL-18-induced myocardial injury include induction of inflammation, increased apoptosis, a cardiac hypertrophy effect, modulation of mitogen activated protein kinase activation, and changes in intracellular calcium. Finally, we briefly reviewed the therapeutic strategies for inhibiting IL-18's biological activity to protect cardiac tissue from injury.

引用

页码：3 / 10

页数：8

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