Abstract
Myocardial infarction (MI) remains one of the leading causes of death worldwide. Inflammation and immune responses after MI are of significance to the adverse cardiac remodeling. Regulatory T cells (Tregs) play an important role in suppressing the immune response and thus benefit the post-MI remodeling. After MI, damaged cardiomyocytes may be replaced by scar tissue, leading to systolic and diastolic dysfunction and subsequently adverse remodeling. In this review, we provide an overview of the function and possible mechanisms of Tregs in post-MI heart repair. Specifically, after the occurrence of MI, Tregs infiltrated to peri-infarcted myocardium through CCR5 pathway, CXCR4-CXCL12 axis, and Hippo pathway. Normal functional Tregs can reduce the size of the MI area, improve heart function, and ameliorate myocardial remodeling by inhibiting proinflammatory cells accumulation, changing the proportion of macrophages phenotypes, improving myocardial fibrosis, protecting myocardial cells, and promoting angiogenesis. Eventually, Functional Tregs recruited into the heart can improve MI outcomes. Therefore, targeted therapies with Tregs might provide a promising approach to the treatment of MI remodeling.
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