IL33 and myocardial infarction: Its loss compromises myocardial integrity, increasing susceptibility to hypertrophy and fibrosis after pressure overload and worsening outcomes following myocardial infarction by removing its inhibitory effect on cardiomyocyte apoptosis and its support for recovery.32,36,37 Beyond the heart, systemic blockade may disrupt immune regulation, as IL-33 promotes the function and clonal expansion of regulatory T cells; impaired signaling has been clinically linked to conditions such as inflammatory bowel disease.