Myocardial infarction (MI) remains one of the leading causes of heart failure development and death worldwide. To date, interventional and pharmacological therapies are effective in reducing the onset of heart failure and promoting survival. However, progressive maladaptive remodeling post-MI persists in a large fraction of patients resulting in poor prognosis. Immune cell responses and an inflammatory environment largely contribute to adverse cardiac remodeling post-MI. CD4FOXP3 regulatory T cells (Tregs) are known for their immunosuppressive capacity and have been successfully implemented in multiple preclinical studies of permanent and ischemia-reperfusion MI. In this review, we highlight the important cardioprotective role of Tregs at the cardiac tissue, cellular, and molecular level, as well as the most prominent pharmacological venues that could be used to exploit Tregs as a novel therapeutic intervention to lessen myocardial injury post-MI.