IL1RL1 and myocardial infarction: Following augmented cardiac loads (augmented pressure and biomechanical stress, and tension of the muscular structures) associated with acute myocardial infarction (AMI) or progressive heart failure (HF), cardiomyocytes, endothelial cells and cardiac fibroblasts increase the expression and release of both ST2 forms and IL-33 [4,28,29].