Article (Published version) (236 Kb) - Limited access to UNIGE
When are pro-inflammatory cytokines SAFE in heart failure?
|Published in||European Heart Journal. 2011, vol. 32, no. 6, p. 680-5|
|Abstract||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.|
|Keywords||Animals — Cardiotonic Agents/pharmacology — Cytokines/metabolism/physiology — Disease Models, Animal — Heart Failure/etiology/prevention & control/therapy — Humans — Interleukin-6/metabolism — Mice — Rats — Receptors, Cytokine/physiology — STAT3 Transcription Factor/metabolism — Signal Transduction/physiology — Tumor Necrosis Factors/metabolism|
|Research group||Lipoprotéines sériques (598)|
|LECOUR, Sandrine, JAMES, Richard William. When are pro-inflammatory cytokines SAFE in heart failure?. In: European Heart Journal, 2011, vol. 32, n° 6, p. 680-5. https://archive-ouverte.unige.ch/unige:24173|