Inflammation and Inflammatory Cells in Myocardial Infarction and Reperfusion Injury: A Double-Edged Sword.
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.
Department of Burns and Cutaneous Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi, China.; Department of Immunology, State Key Laboratory of Cancer Biology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Jiaqi
J
Liu
Clinical Skill Training Center, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Haijuan
H
Wang
Department of Physiology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Jun
J
Li
inflammation; macrophage; myocardial infarction; reperfusion injury; toll-like receptor