Background: Acute myocardial infarction (AMI) pathophysiology is mediated by systemic, intraplaque myocardial inflammatory processes that occur mainly due to coronary artery thrombosis in an atherosclerotic plaque area. The G-protein-coupled chemokine receptor (Ccr6) is displayed on the surface of many types of leukocytes, that have been found in atherosclerotic plaques. It is a novel mediator of inflammation and immune response.
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