“…Soluble ST2 (sST2) acts as a decoy receptor, directly bound to IL-33, and suppresses activation of JNK (c-Jun N-terminal kinase), NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) and ERK (extracellular signalregulated kinases), reversing the beneficial effects of the IL-33/ST2 system, thus destabilizing the defense mechanism. The association between sST2 and mortality rates was confirmed in patients with acute [10][11][12][13], chronic decompensated [14] and chronic HF [3,15,16]. Moreover, the association was observed regardless of the left ventricular ejection fraction (LVEF) values, as well as in patients with reduced ejection fraction (HFrEF) [3,17,18].…”