Dendritic Cells in the Immunoregulation of Myocardial Infarction: Mechanisms and Therapeutic Strategies

Myocardial infarction (MI) remains a leading cause of mortality and long-term disability worldwide. Its pathological process involves multiple interconnected stages, including atherosclerosis, ischemia-reperfusion injury, ventricular remodeling, and fibrosis. Dendritic cells (DCs), as key antigen-presenting cells bridging innate and adaptive immunity, exert bidirectional immunoregulatory functions in the pathogenesis of MI. During atherogenesis, DCs actively participate in lipid deposition, foam cell formation, and inflammatory regulation. Following MI, DCs influence myocardial injury and repair through diverse mechanisms, including cytokine secretion, T cell differentiation modulation, and exosome-mediated intercellular communication. Clinical studies have revealed a marked reduction in circulating DCs in MI patients, accompanied by functional hyperactivation of the residual DC population, which correlates closely with adverse clinical outcomes. On the therapeutic front, several DC-targeted strategies have demonstrated efficacy in preclinical models, including the C-X-C motif chemokine receptor 4 antagonists POL5551 and POL6326, mannosylated cytotoxic T-lymphocyte-associated protein 4-presenting small extracellular vesicles (CM@sEVs), tolerogenic dendritic cells (tDCs), and DC-derived exosomes (Dex), all of which have shown potential to improve cardiac function, attenuate fibrosis, and promote angiogenesis. Additionally, conventional medications such as statins and angiotensin-converting enzyme inhibitors can also modulate DC functions to confer cardioprotection. This review provides a comprehensive overview of the immunoregulatory mechanisms of DCs across the pathological spectrum of MI and highlights recent progress in DC-based therapeutic strategies, aiming to provide a theoretical foundation for the immunotargeted treatment of MI.