Trained immunity in myocardial infarction: From mechanisms to translational potential

Myocardial infarction (MI) ranks among the leading causes of death globally, with its prognosis closely linked to inflammatory responses. Both excessive early inflammation and persistent residual inflammation lead to adverse cardiac remodeling and heart failure. In recent years, the role of trained immunity in cardiovascular risk factors and MI-associated inflammatory responses has garnered increasing attention. Cardiovascular risk factors can induce trained immunity, placing the body in a "preactivated" innate immune state prior to MI occurrence. This state is further amplified upon myocardial necrosis, triggering excessive inflammation. Additionally, MI itself can induce trained immunity, leading to long-term inflammatory memory and residual inflammation risk. Targeting metabolic and epigenetic pathways of trained immunity offers approaches for post-MI anti-inflammatory interventions. A comprehensive understanding of trained immunity's mechanisms in MI holds promise for establishing theoretical foundations and translational directions for precision anti-inflammatory therapies and improving long-term patient outcomes.