ArticleBMC cardiovascular disorders2024
LY86 facilitates ox-LDL-induced lipid accumulation in macrophages by upregulating SREBP2/HMGCR expression.
Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.Nature communications · 2026Article
- Transcriptomic insights into the co-occurring psychological symptoms and cardiovascular risks among military service members and veterans with mild traumatic brain injury: A LIMBIC-CENC study.Brain, behavior, & immunity - health · 2026Article
- Genetically supported mediators linking peripheral metabolism to cerebral ischemia: a multi-omics characterization of HMGCR, TLR4, and MMP9 in angina pectoris and stroke.Briefings in functional genomics · 2026Article
- Identification of Novel Biomarkers of Bacterial Lipopolysaccharides in Diabetic Nephropathy via Transcriptomics and Mendelian Randomization.Current gene therapy · 2026Article
- Enhanced lymphocyte infiltration in the liver of LDL receptor and Myeloid Differentiation 1 double knockout mice on high fat diet.Scientific reports · 2025Article
- Non-linear association between low-density lipoprotein cholesterol and risk of prediabetes: a retrospective cohort study based on Chinese adults.Frontiers in endocrinology · 2025Observational
- Identification and verification of key molecules in the epileptogenic process of focal cortical dysplasia.Metabolic brain disease · 2024Article
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Authors and funding
6 authors.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.