Inflammation and repair in the ischaemic myocardium.
Shortly after myocardial infarction, various circulating leukocyte subsets accumulate in the heart. Leukocyte recruitment is highly coordinated and relies on cell production in the bone marrow, mobilization to the blood, and chemokine-mediated infiltration to the destination tissue. Neutrophils, which are phagocytic and inflammatory, are among the first leukocytes to accumulate in large numbers. Within a day, neutrophils disappear and are replaced by a subset of monocytes that further contribute to inflammation and phagocytosis. After a few days, monocyte-derived reparative macrophages accrue, quell inflammation, and foster angiogenesis and tissue remodelling. Studies suggest a well-balanced response comprising these three waves is essential to optimal infarct healing.
Filip K. Swirski, Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston,, MA 02114, USA, E-mail: fswirski@mgh.harvard.edu.
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D000818:Animals; D006487:Hemostasis / Q000276:immunology; D006801:Humans; D008264:Macrophages / Q000276:immunology*; D008955:Models, Cardiovascular; D018448:Models, Immunological; D009000:Monocytes / Q000276:immunology*; D017202:Myocardial Ischemia / Q000276:immunology* / Q000473:pathology; D009205:Myocarditis / Q000276:immunology* / Q000473:pathology; D018375:Neutrophil Activation / Q000276:immunology; D009504:Neutrophils / Q000276:immunology*; D012038:Regeneration / Q000276:immunology*
Inflammation; myocardium