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- W162000243 abstract "Myocardial infarction is associated with an inflammatory reaction, which is a prerequisite for healing and scar formation 1-3 Myocardial cell necrosis results in the release of subcellular membrane constituents, rich in mitochondria, which are capable of activating the complement cascade.4,5 This represents the initial chemotactic event responsible for neutrophil influx in the ischemic myocardium. Subsequently, activated neutrophils adhere to the endothelium and transmigrate to the extravascular space. Neutrophils accumulating in the ischemic areas release proteolytic enzymes or reactive oxygen species, injuring surrounding myocytes. However, in vivo, these toxic products are almost exclusively secreted by adherent neutrophils. Neutrophil adhesion to cardiac myocytes is dependent on neutrophil integrin activation and on the induction of Intercellular Adhesion Molecule-I (ICAM-I) on cardiac myocytes.6-8 Myocyte ICAM-1 induction is dependent on a cytokine cascade leading to IL-6 expression in mononuclear cells9 and myocytes.1O Cardiac mast cells appear to have a significant role in initiating this cytokine cascade,9 and may also serve as important sources of fibrogenic factors during healing of a reperfused myocardial infarct.11" @default.
- W162000243 created "2016-06-24" @default.
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- W162000243 date "2003-01-01" @default.
- W162000243 modified "2023-09-23" @default.
- W162000243 title "Mast Cells in Experimental Myocardial Infarction" @default.
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- W162000243 doi "https://doi.org/10.1007/978-1-4419-9264-2_11" @default.
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