Abstract
Ischemic heart disease is a common condition and a leading cause of mortality and morbidity. Macrophages, besides their role in host defense and tissue homeostasis, are critical players in the pathophysiological processes induced by myocardial infarction. In this article we will summarize the current understanding of the role of monocytes and macrophages in myocardial damage and cardiac remodeling in relation to their origin and developmental paths. Furthermore, we describe their potential implications in therapeutic strategies to modulate myocardial healing and regeneration.
Highlights
Cardiac diseases, especially acute myocardial infarction and congestive heart failure, are among the most frequent causes of death in the western world and are on the uprise in developing countries
In addition to the recruitment of blood derived monocytes, tissueresident macrophages in the heart represent another source of innate immune cells, which likely contribute to a local inflammatory process in the ischemic myocardium (Epelman et al, 2014a)
There is no doubt that future studies will reveal the precise contribution of monocyte/macrophage populations to myocardial remodeling in pathological conditions thereby integrating findings on their developmental origin and regulation
Summary
Especially acute myocardial infarction and congestive heart failure, are among the most frequent causes of death in the western world and are on the uprise in developing countries. A broad spectrum of local and systemic mechanisms are initiated in myocardial infarction and contribute to cardiac remodeling. If uncontrolled, they may lead to negative changes in the geometry, structure and function of the ventricle and may have deleterious effects on cardiac function in the long term. Macrophages are an integral part of the innate immune response They are equipped with an array of pathogen recognition receptors which can activate phagocytosis of pathogens and the secretion of cytokines and chemokines. In this review we will summarize the functions of monocytes and macrophages in myocardial infarction and outline potential therapeutic strategies to improve infarct healing and outcome by manipulating distinct subsets of mononuclear phagocytes
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