Journal
CLINICAL MEDICINE INSIGHTS-CARDIOLOGY
Volume 10, Issue -, Pages 79-84Publisher
SAGE PUBLICATIONS LTD
DOI: 10.4137/CMC.S33164
Keywords
myocardial infarction; reperfusion injury; inflammation; toll-like receptor; macrophage
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Funding
- National Natural Science Foundation of China [81000088]
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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.
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