Apoptotic Processes in Atherosclerosis Mechanisms
Summary
Atherosclerosis arises from the build-up of lipid-laden plaques within arterial walls, a process in which programmed cell death (apoptosis) plays a central role. In early lesions, apoptosis of macrophages and smooth muscle cells limits lesion growth by reducing cellularity, whereas in advanced plaques defective clearance of apoptotic debris fuels inflammation, necrotic core formation and fibrous cap thinning. Efficient phagocytic removal of dying cells, termed efferocytosis, is orchestrated by receptors such as MerTK and by bridging molecules that link exposed phosphatidylserine on apoptotic membranes to phagocyte receptors. When efferocytosis fails, secondary necrosis liberates pro-inflammatory mediators and oxidised lipid species, exacerbating plaque instability. Endoplasmic reticulum stress, mitochondrial dysfunction and disturbed haemodynamic forces further modulate apoptotic signalling and efferocytic capacity within endothelial cells, smooth muscle cells and lesional macrophages. Understanding the molecular crosstalk between apoptosis, efferocytosis and inflammatory resolution has revealed novel targets for stabilising vulnerable plaques and preventing acute cardiovascular events.
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Apoptotic Processes in Atherosclerosis Mechanisms publication trend
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Technical terms
Apoptosis: A form of programmed cell death characterised by membrane blebbing and DNA fragmentation, which normally proceeds without provoking inflammation.
Efferocytosis: The phagocytic clearance of apoptotic cells by macrophages and other phagocytes, essential for resolution of inflammation.
MerTK: A receptor tyrosine kinase on phagocytes that recognises apoptotic cells via bridging ligands, promoting efferocytosis and anti-inflammatory signalling.
Necrotic core: The lipid-rich, cell debris-filled central region of advanced atherosclerotic plaques, whose enlargement destabilises the plaque.
Endoplasmic reticulum stress: A cellular state triggered by accumulation of misfolded proteins in the ER, which can induce apoptosis through UPR (unfolded protein response) pathways.
References
- Enhancing CAR Macrophage Efferocytosis Via Surface Engineered Lipid Nanoparticles Targeting LXR Signaling. Advanced Materials (2024).
- Disturbed flow impairs MerTK-mediated efferocytosis in aortic endothelial cells during atherosclerosis. Theranostics (2024).
- Efferocyte‐Derived MCTRs Metabolically Prime Macrophages for Continual Efferocytosis via Rac1‐Mediated Activation of Glycolysis. Advanced Science (2023).
- Mechanisms and Consequences of Defective Efferocytosis in Atherosclerosis. Frontiers in Cardiovascular Medicine (2018).
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