Acute myocardial infarction alters the macrophage phenotype and supply chain from tissue resident to blood monocytes, increasing systemic leucocyte supply and associating with cardiovascular mortality.
This review highlights how acute myocardial infarction alters innate immune cell pathways, increasing systemic leucocyte supply which is closely associated with cardiovascular mortality.
Knowledge of macrophages in steady-state and diseased tissue is rapidly expanding, propelled by improved diagnostic capacity to detect and monitor cells in their native environments. In this review, we discuss implications for ischaemic heart disease and examine innate immune cell pathways that increase systemic leucocyte supply after myocardial infarction (MI). Acute MI alters the macrophage phenotype and supply chain from tissue resident to blood monocytes sourced from haematopoietic organs. That blood leucocytosis closely associates with cardiovascular mortality provides a strong motivation to understand why and how organ ischaemia alters cellular immunity.
Nahrendorf et al. (Tue,) conducted a review in Ischaemic heart disease and myocardial infarction. Innate immune cell pathways was evaluated. Acute myocardial infarction alters the macrophage phenotype and supply chain from tissue resident to blood monocytes, increasing systemic leucocyte supply and associating with cardiovascular mortality.
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