Journal
FRONTIERS IN CARDIOVASCULAR MEDICINE
Volume 4, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcvm.2017.00086
Keywords
efferocytosis; atherosclerosis; inflammation resolution; macrophages; post-apoptotic necrosis
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Funding
- American Federation for Aging Research [A16034]
- American Heart Association Fellow-to-Faculty grant [17FTF33660643]
- NIH [T32 HL007343-28, R00 HL119587, R01s HL075662, HL127464, HL132412]
- [15POST25620024]
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Efficient clearance of apoptotic cells, termed efferocytosis, critically regulates normal homeostasis whereas defective uptake of apoptotic cells results in chronic and nonresolving inflammatory diseases, such as advanced atherosclerosis. Monocyte-derived macrophages recruited into developing atherosclerotic lesions initially display efficient efferocytosis and temper inflammatory responses, processes that restrict plaque progression. However, during the course of plaque development, macrophages undergo cellular reprogramming that reduces efferocytic capacity, which results in post-apoptotic necrosis of apoptotic cells and inflammation. Furthermore, defective efferocytosis in advanced atherosclerosis is a major driver of necrotic core formation, which can trigger plaque rupture and acute thrombotic cardiovascular events. In this review, we discuss the molecular and cellular mechanisms that regulate efferocytosis, how efferocytosis promotes the resolution of inflammation, and how defective efferocytosis leads to the formation of clinically dangerous atherosclerotic plaques.
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