Journal
EUROPEAN HEART JOURNAL
Volume 32, Issue 6, Pages 680-+Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehq484
Keywords
Heart failure; Pro-inflammatory cytokines; Tumour necrosis factor alpha; Signal transducer and activator of transcription; Prosurvival pathways
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Funding
- South African Medical Research Council (MRC)
- National Research Foundation, MRC Cape Heart Group
- Swiss South African Joint Research Programme [JRP-16]
- Swiss National Research Foundation [31-118418]
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The cytokine hypothesis presently suggests that an excessive production of pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF) and interleukin 6 (IL6), contributes to the pathogenesis of heart failure. The concept, successfully proved in genetically modified animal models, failed to translate to humans. Recently, accumulation of apparently paradoxical experimental data demonstrates that, under certain conditions, production of pro-inflammatory cytokines can initiate the activation of a pro-survival cardioprotective signalling pathway. This novel path that involves the activation of a transcription factor, signal transducer and activator of transcription 3 (STAT3), has been termed the survival activating factor enhancement (SAFE) pathway. In this review, we will discuss whether targeting the SAFE pathway may be considered as a preventive and/or therapeutic measure for the treatment of heart failure.
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