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LY86 facilitates ox-LDL-induced lipid accumulation in macrophages by upregulating SREBP2/HMGCR expression

Jiang, Guangwei, Li, Jikuan, Niu, Shuai, Dong, Ruoyu, Chen, Yuyan, Bi, Wei·2024·BMC Cardiovascular Disorders
DOI 10.1186/s12872-024-03957-1PMC PMC11140969
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Abstract

LY86, also known as MD1, has been implicated in various pathophysiological processes including inflammation, obesity, insulin resistance, and immunoregulation. However, the role of LY86 in cholesterol metabolism remains incompletely understood. Several studies have reported significant up-regulation of LY86 mRNA in atherosclerosis; nevertheless, the regulatory mechanism by which LY86 is involved in this disease remains unclear. In this study, we aimed to investigate whether LY86 affects ox-LDL-induced lipid accumulation in macrophages. Firstly, we confirmed that LY86 is indeed involved in the process of atherosclerosis and found high expression levels of LY86 in human atherosclerotic plaque tissue. Furthermore, our findings suggest that LY86 may mediate intracellular lipid accumulation induced by ox-LDL through the SREBP2/HMGCR pathway. This mechanism could be associated with increased cholesterol synthesis resulting from enhanced endoplasmic reticulum stress response.

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Metadata

Authors
Jiang, G., Li, J., Niu, S., Dong, R., Chen, Y., & Bi, W.
Venue
BMC Cardiovascular Disorders
Publisher
Springer Science and Business Media LLC
Published
2024-05-31
Volume
24
Issue
1
ISSN
1471-2261
DOI
10.1186/s12872-024-03957-1
PMC
PMC11140969
Cited by
12
References
0
Language
en
Licence
Funders
Hebei Medical Science Research Project (20190383)

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