Interleukin 18 and cardiovascular disease in HIV-1 infection: a partner in crime?
Cardiovascular disease has been frequent in HIV-infected patients both before and after the advent of antiretroviral therapy (HAART). The pathogenic basis for the increase of cardiovascular disease, in particular myocardial lesions, may involve HIV-1 itself or other mechanisms including endothelial dysfunction, activation of proinflammatory cytokines, and changes in platelets, which lead to atherosclerotic lesions of blood vessels. In the last decade, among the proinflammatory cytokines, interleukin 18 seems to play a central role in the inflammatory cascade, leading to development of atherosclerotic disease and the occurrence of ischemic heart disease in uninfected HIV-1 people. Increased levels of interleukin 18 were observed in HIV-1 infected patients. This review attempts to evaluate the role of interleukin 18 in cardiovascular disease, especially in myocardial infarction, in HIV-1 infection, as well as the relationship between interleukin 18 and atherosclerotic plaque formation. Two other characteristic aspects in HIV-1 infection, metabolic syndrome and lipodystrophy, will be evaluated in light of activity of interleukin 18. Moreover, the role of platelets and interleukin 18 as an important linkage between chronic inflammation, endothelial dysfunction, and atherogenesis will be highlighted. Finally, experimental an animal model of rhesus macaques infected with simian immunodeficiency virus clearly demonstrates the involvement of interleukin 18 in myocardial lesions, and that circulating levels of interleukin 18 are important predictors of coronary heart disease. In conclusion, interleukin 18 may be considered a partner in crime with other factors, including endothelial dysfunction, increased expression and production of adhesion molecules and proinflammatory cytokines in determining cardiovascular disease.[1]References
- Interleukin 18 and cardiovascular disease in HIV-1 infection: a partner in crime? Torre, D., Pugliese, A. AIDS. Rev (2010) [Pubmed]
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