Cardiac injury can lead to cardiomyocyte death, intense inflammation, scar formation and, over time, adverse cardiac remodelling.
Following injury, cardiac inflammation is triggered by the release of conserved endogenous molecules and the production of pro-inflammatory cytokines and chemokines that lead to cellular infiltration.
Early activation of mast cells leads to neutrophil recruitment, a robust inflammatory response and tissue damage.
Recruited monocytes and resident macrophages modulate both tissue injury and tissue healing.
Macrophage origin may dictate function in the heart. Primitive embryonically derived macrophages mediate cardiac tissue repair, whereas bone marrow-derived monocytes contribute to inflammation following cardiac injury.
Lymphocytes and macrophages are involved in the complex transition from initial cardiac tissue inflammation to wound healing.
Despite the advances that have been made in developing new therapeutics, cardiovascular disease remains the leading cause of worldwide mortality. Therefore, understanding the mechanisms underlying cardiovascular tissue injury and repair is of prime importance. Following cardiac tissue injury, the immune system has an important and complex role in driving both the acute inflammatory response and the regenerative response. This Review summarizes the role of the immune system in cardiovascular disease — focusing on the idea that the immune system evolved to promote tissue homeostasis following injury and/or infection, and that the inherent cost of this evolutionary development is unwanted inflammatory damage.
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The authors declare no competing financial interests.
- Granulation tissue
This is tissue that arises after cardiac tissue injury, when the replacement of cardiomyocytes with collagen and extracellular matrix occurs in order to maintain the integrity of the myocardial wall.
- Innate B cells
These cells are thought to become rapidly activated in the absence of classical T cell-dependent antigen presentation mechanisms. They are mobilized by other cell types and/or inflammatory triggers.
- ApoE-deficient mice
These mice are used to model atherosclerosis. They have increased total plasma cholesterol levels and increased bone marrow production of monocytes and heightened inflammatory responses.
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Epelman, S., Liu, P. & Mann, D. Role of innate and adaptive immune mechanisms in cardiac injury and repair. Nat Rev Immunol 15, 117–129 (2015). https://doi.org/10.1038/nri3800
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