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

Journal

HEART FAILURE REVIEWS
Volume 14, Issue 2, Pages 113-123

Publisher

SPRINGER
DOI: 10.1007/s10741-008-9104-z

Keywords

Heart failure; Oxidative stress; Antioxidants; Inflammation

Funding

  1. Circulatory Respiratory Institute of the CIHR, Canada
  2. University of Manitob
  3. Manitoba Health Research Council
  4. Heart Foundation

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Our understanding of the multiple in vivo functions of the proinflammatory cytokine, tumor necrosis factor (TNF alpha), is advancing at a rapid pace. In addition to its antitumor effects, overproduction of TNF alpha provokes tissue injury and organ failure. TNF alpha has also been shown to be cardiodepressent and responsible for various cardiovascular complications. It appears that still much needs to be learned for a full comprehension of the role of TNF alpha 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 TNF alpha. IL-10 suppresses the production of TNF alpha and many other proinflammatory cytokines. TNF alpha-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 TNF alpha may be a new therapeutic strategy for a healthier heart.

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