Inflammation and Inflammatory Cells in Myocardial Infarction and Reperfusion Injury: A Double-Edged Sword

Abstract

Myocardial infarction (MI) is the most common cause of cardiac injury, and subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Therefore, inflammation and inflammatory cell infiltration are the hallmarks of MI and reperfusion injury. Ischemic cardiac injury activates the innate immune response via toll-like receptors and upregulates chemokine and cytokine expressions in the infarcted heart. The recruitment of inflammatory cells is a dynamic and superbly orchestrated process. Sequential infiltration of the injured myocardium with neutrophils, monocytes and their descendant macrophages, dendritic cells, and lymphocytes contributes to the initiation and resolution of inflammation, infarct healing, angiogenesis, and ventricular remodeling. Both detrimental effects and a beneficial role in the pathophysiology of MI and reperfusion injury may be attributed to the subset heterogeneity and functional diversity of these inflammatory cells.

Keywords: inflammation; macrophage; myocardial infarction; reperfusion injury; toll-like receptor.

Figure 1

Diverse roles of inflammation and inflammatory cells in the pathophysiology of MI and reperfusion injury. Inflammation is not only involved in reperfusion injury and postinfarction remodeling but is also integral to wound healing and tissue repair after MI. Inflammatory cell subsets and function heterogeneity account for both the detrimental and beneficial roles of monocytes/macrophages, DCs, and lymphocytes in the pathophysiology of reperfusion injury and infarct healing.