Abstract
During homeostasis, immune cells perform daily housekeeping functions to maintain heart health by acting as sentinels for tissue damage and foreign particles. Resident immune cells compose 5% of the cellular population in healthy human ventricular tissue. In response to injury, there is an increase in inflammation within the heart due to the influx of immune cells. Some of the most common immune cells recruited to the heart are macrophages, dendritic cells, neutrophils, and T-cells. In this review, we will discuss what is known about cardiac immune cell heterogeneity during homeostasis, how these cell populations change in response to a pathology such as myocardial infarction or pressure overload, and what stimuli are regulating these processes. In addition, we will summarize technologies used to evaluate cell heterogeneity in models of cardiovascular disease.
Highlights
Chaos: Deciphering Immune CellThe healthy mammalian heart contains an estimated 2–3 billion cardiac myocytes, which is approximately 75% of normal myocardial tissue volume but only one third of total cell numbers [1,2]
Cardiac remodeling in diseased hearts is temporal and spatially dependent with unresolved or mistimed inflammation leading to excessive matrix degradation and cardiac rupture, dilation of the left ventricle (LV), or development of heart failure [11,12]
When T-cells were replenished (RAG2−/− with CD3+ cells), levels of both proLOX and lysyl oxidase (LOX) protein were significantly increased [61]. Other crosslinks, such as those generated by transglutaminase and by advanced glycation end products (AGEs), play an important role in the fibrotic myocardium, but it is not currently known if T-cells are a primary effector of these crosslinks in response to pressure overload (PO)
Summary
The healthy mammalian heart contains an estimated 2–3 billion cardiac myocytes, which is approximately 75% of normal myocardial tissue volume but only one third of total cell numbers [1,2]. In response to injury after myocardial infarction (MI), there is an increase in inflammation within the heart due to the influx of immune cells. Some of the most common immune cells recruited to the heart are macrophages, dendritic cells, monocytes, neutrophils, and Tcells [1,5]. Biomolecules 2022, 12, 11 focus to include the role of immune cells in regulating HFpEF pathology. In models of pressure overload (PO), resident and recruited macrophages, play a role in fibrotic development through activation of other cell types. There has been a shift in the focus to include the role of immune cells in regulating HFpEF pathology. While the role of immune cells post-MI is better understood, fewer studies have focused on how these immune cells regulate each other in the heart before and after PO
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