Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Area of Science:

• Cardiovascular Research
• Immunology
• Cell Biology

Background:

• Atherosclerosis is a chronic inflammatory condition characterized by myeloid cell infiltration into the vessel wall.
• While lymphocytes and platelets were historically implicated, recent research highlights the critical role of myeloid leukocytes.
• Key myeloid cell types include monocyte subsets, neutrophils, dendritic cells, and endothelial progenitor cells.

Purpose of the Study:

• To review the multifaceted roles of various myeloid cell types in atherosclerosis.
• To examine the specific impact of hyperlipidaemia on myeloid cell function and behavior.
• To elucidate how myeloid cells initiate and perpetuate atherosclerotic plaque development and destabilization.

Main Methods:

• Literature review focusing on myeloid cell involvement in atherosclerosis.
• Analysis of studies investigating the effects of hyperlipidaemia on myeloid cell homeostasis and phenotype.
• Synthesis of current understanding regarding myeloid cell transcriptional regulation and extravasation.

Main Results:

• Myeloid cells are central to initiating and perpetuating atherosclerotic plaque formation and destabilization.
• Hyperlipidaemia disrupts myeloid cell hemostasis, alters their phenotype, and affects pro-inflammatory gene regulation.
• These alterations promote myeloid cell extravasation, contributing significantly to atherosclerosis.

Conclusions:

• Myeloid cells play a pivotal role in the pathogenesis of atherosclerosis.
• Hyperlipidaemia exacerbates atherosclerosis by dysregulating myeloid cell functions.
• Targeting myeloid cell pathways presents a potential therapeutic strategy for atherosclerosis.