Apolipoprotein E and Atherosclerosis Mechanisms

Summary

Apolipoprotein E (apoE) plays a central role in lipid metabolism and the pathogenesis of atherosclerosis. It functions as a ligand for members of the low-density lipoprotein receptor family, thereby mediating the clearance of atherogenic lipoproteins from the circulation. Beyond lipoprotein clearance, apoE regulates cholesterol efflux from macrophage foam cells and orchestrates reverse cholesterol transport to the liver for excretion. Emerging evidence highlights apoE’s influence on immune cell function, including modulation of monocyte activation, control of haematopoiesis and regulation of microRNA-dependent signalling pathways within the vascular wall. Genetic variants of apoE are known to differentially affect plasma lipid profiles and cardiovascular risk, while apoE-deficient and isoform knock-in mouse models have elucidated mechanisms of plaque initiation, progression and regression. Interactions between apoE, inflammation and extracellular vesicle release further underscore its multifaceted atheroprotective properties. Insights into these mechanisms have global significance for the development of therapeutic strategies, such as apoE-mimetic peptides, gene therapy approaches and modulation of lymphatic function, aimed at reducing the burden of cardiovascular disease.

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Apolipoprotein E and Atherosclerosis Mechanisms publication trend

The graph below shows the total number of articles in apolipoprotein e and atherosclerosis mechanisms across all publications each year (not limited to Nature Index journals).

Technical terms

Apolipoprotein E (apoE): A lipid-binding protein that mediates the clearance of atherogenic lipoproteins and regulates cholesterol efflux.

Atherosclerosis: A chronic condition characterised by the accumulation of lipid-laden plaques in arterial walls.

Foam cell: A macrophage engorged with lipids that contributes to plaque formation.

Reverse cholesterol transport: A process by which excess cholesterol is transported from peripheral tissues to the liver for elimination.

MicroRNA: Short non-coding RNA molecules that downregulate gene expression at the post-transcriptional level.

References

  1. Characterization of Atherosclerotic Mice Reveals a Sex-Dependent Susceptibility to Plaque Calcification but No Major Changes in the Lymphatics in the Arterial Wall. International Journal of Molecular Sciences (2024).
  2. Apoprotein E and Reverse Cholesterol Transport. International Journal of Molecular Sciences (2018).
  3. Apolipoprotein E and Atherosclerosis: From Lipoprotein Metabolism to MicroRNA Control of Inflammation. Journal of Cardiovascular Development and Disease (2018).
  4. ApoE knockout and knockin mice: the history of their contribution to the understanding of atherogenesis. Journal of Lipid Research (2016).

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