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Editorial
. 2023 May 11;11(5):1424.
doi: 10.3390/biomedicines11051424.

Lipids and Lipoproteins in Atherosclerosis

Evgeny Bezsonov  1   2   3 , Victoria Khotina  1 , Victor Glanz  2 , Igor Sobenin  4 , Alexander Orekhov  1   2
Affiliations
Editorial

Lipids and Lipoproteins in Atherosclerosis

Evgeny Bezsonov et al. Biomedicines. .

Abstract

Atherosclerosis is a chronic inflammatory disease [...].

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The role of LDL desialylation in atherosclerosis development. (A) The structure of sialic acid-containing glycosylation of protein, and the mechanism of the removal of sialic acid residue [16]. (B) The formation of desialylated LDL, leading to its self-association and intracellular accumulation [16]. The activity of trans-sialidase, discovered in human serum by Vladimir Tertov, could result in the generation of desialylated LDL (by using native LDL as a donor of sialic acid residue for its further transport to the acceptor molecule). The impaired activity of cellular sialyltransferases could also potentially result in reduced sialylation of LDL (in comparison with native LDL). (C) The mechanism of elevated expression of NEU1 in monocytes/macrophages (including the ones located in atherosclerotic lesions) after pro-inflammatory stimulation [19]. Lipopolysaccharide (LPS) and IL1𝛽 induce elevated expression of NEU1 in the monocyte-like THP-1 cell line. Macrophages in the intima layer, calcified regions, and the adventitia of atherosclerotic plaque also have elevated levels of Neu1 [19]. If the elevated Neu1 protein in monocytes/macrophages obtains access to native LDL, then it could become a self-perpetuating mechanism of the generation of desialylated LDL (since modified LDL can also be a trigger of pro-inflammatory activation of immune cells).
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