Likewise, the functional ligand of ST2 (interleukin-33; IL-33) is released from cardiac fibroblasts in response to damage, and its interaction with ST2L mediates a cardioprotective mechanism that counteracts cardiac hypertrophy and fibrosis, reduces apoptosis, and improves myocardial function [39, 40, 44]. Here, IL1RL1 is linked to cardiac hypertrophy.