Cardiac Macrophage Biology in the Steady State Heart, the Aging Heart, and Following Myocardial Infarction

Publication date: Available online 13 October 2017
Source:Translational Research
Author(s): Yonggang Ma, Alan J. Mouton, Merry L. Lindsey
Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a pro-inflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both pro- and anti- inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a pro-inflammatory M1 phenotype early and become polarized towards an anti-inflammatory M2 phenotype later post-MI. While this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.



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