Summary
PROJECT SUMMARY Ischemic heart disease following myocardial infarction (MI) is a leading cause of global morbidity and mortality. During MI, infiltrating immune cells, particularly monocytes, differentiate into macrophages, adopting both reparative and maladaptive pro-inflammatory roles. These maladaptive immune responses can drive chronic inflammation, adverse remodeling, and ultimately heart failure (HF) progression. Although blocking monocyte recruitment has been explored as a therapeutic strategy, this approach risks impairing the essential reparative functions required for proper wound he
