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Heart Fail Rev. 2009 Jun;14(2):113-23. doi: 10.1007/s10741-008-9104-z. Epub 2008 Aug 19.

Biology of TNFalpha and IL-10, and their imbalance in heart failure.

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  • 1Department of Pharmacology, The University of Michigan, Ann Arbor, MI 48105, USA.


Our understanding of the multiple in vivo functions of the proinflammatory cytokine, tumor necrosis factor (TNFalpha), is advancing at a rapid pace. In addition to its antitumor effects, overproduction of TNFalpha provokes tissue injury and organ failure. TNFalpha has also been shown to be cardiodepressant and responsible for various cardiovascular complications. It appears that still much needs to be learned for a full comprehension of the role of TNFalpha in heart biology. Another cytokine, interleukin-10 (IL-10), has been shown to have anti-inflammatory properties. It is suggested to counterbalance many adverse effects of TNFalpha. IL-10 suppresses the production of TNFalpha and many other proinflammatory cytokines. TNFalpha-induced oxidative stress is also known to be mitigated by IL-10. Moreover, improvement in cardiac function after treatment with various drugs is also shown to be associated with an increase in IL-10 content. Based on the data reviewed in here, it is suggested that an optimal balance between IL-10 and TNFalpha may be a new therapeutic strategy for a healthier heart.

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