INTERLEUKIN 18 IN THE HEART. Export

@article{citeulike:2968572, abstract = {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-1beta converting enzyme). Elevated IL-18 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.}, address = {Departments of *Surgery and {\dag}Cellular and Integrative Physiology; and {\ddag}Center for Immunobiology, Indiana University School of Medicine, Indianapolis, Indiana.}, author = {Wang, Meijing and Markel, Troy A. and Meldrum, Daniel R.}, citeulike-article-id = {2968572}, citeulike-linkout-0 = {http://dx.doi.org/10.1097/SHK.0b013e318160f215}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18562922}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18562922}, doi = {10.1097/SHK.0b013e318160f215}, issn = {1073-2322}, journal = {Shock (Augusta, Ga.)}, keywords = {cardiovascular-disease, il-18, il18-review, review}, month = {July}, number = {1}, pages = {3--10}, posted-at = {2008-07-07 06:35:29}, priority = {2}, title = {INTERLEUKIN 18 IN THE HEART.}, url = {http://dx.doi.org/10.1097/SHK.0b013e318160f215}, volume = {30}, year = {2008} }

TY - JOUR ID - citeulike:2968572 L3 - citeulike-article-id:2968572 N2 - 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-1beta converting enzyme). Elevated IL-18 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. IS - 1 JF - Shock (Augusta, Ga.) SN - 1073-2322 AD - Departments of *Surgery and †Cellular and Integrative Physiology; and ‡Center for Immunobiology, Indiana University School of Medicine, Indianapolis, Indiana. EP - 10 TI - INTERLEUKIN 18 IN THE HEART. VL - 30 SP - 3 KW - cardiovascular-disease KW - il-18 KW - il18-review KW - review AU - Wang, Meijing AU - Markel, Troy AU - Meldrum, Daniel PY - 2008/07// UR - http://dx.doi.org/10.1097/SHK.0b013e318160f215 ER -