Cell and tissue markers of atherosclerosis

Atherosclerotic lesions are characterized by various multiple changes at the gene expression levels. However, there are general trends at the cellular and molecular levels. Extracellular matrix remodeling of blood vessels occurs due to an increase in the mRNA levels of the cathepsin and matalloprotease genes, as well as a decrease in the levels of type I and III collagen transcripts. A change in the transcriptional activity of some genes leads to a disruption in the regulation of the smooth muscle cells cytoskeleton and intercellular interaction, which also contributes to the formation of atherosclerotic lesions. Attraction of leukocytes to the arterial walls by cathepsins, chemokines and other markers associated with signaling systems leads to the infiltration of monocytes into the intima. In addition, there is a change in the ratio of apoprotein expression, the prevalence of the expression of some over others, which leads to the cholesterol accumulation and impaired lipid metabolism.

The genes responsible for the accumulation of oxidized low-density lipoproteinare activated, that induces inflammatory responses through Toll-like receptors. High levels of CD36 and CD68 are observed, signaling the infiltration of lesions by macrophages. This review focuses on the recent studies on the transcriptome of atherosclerotic plaque from the human carotid artery. We examined differentially expressed genes of metalloproteases, cathepsins, chemokines and their receptors, lipid metabolism, extracellular matrix components, receptors associated with signaling systems, macrophage and smooth muscle cells markers. Several studies have overlapping results, as well as new genes that have not previously been reported to be associated with atherosclerosis. Studying of atherosclerotic plaque markers and single signaling pathway genes can provide new insights into the pathways involved in the mechanism of atherogenesis, as well as identify potential biomarkers that characterize the stages of atherosclerotic lesion development.

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