ArticleArteriosclerosis, thrombosis, and vascular biology2025
Inhibition of LXR Signaling in Human Foam Cells Impairs Macrophage-to-Endothelial Cell Cross Talk and Promotes Endothelial Cell Inflammation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Review
- Mechanistic insights into the multi-target anti-atherosclerotic actions of rhubarb: a traditional remedy revisited.Chinese medicine · 2025Review
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16 authors.
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Abstract
backgroundDuring atherogenesis, macrophages turn into foam cells by engulfing lipids present within the atheroma plaques. The shift of foam cells toward proinflammatory or anti-inflammatory phenotypes, a critical step in disease progression, is still poorly understood. LXRs (liver X receptors) play a pivotal role in the macrophage response to lipid, promoting the expression of key genes of cholesterol efflux, mitigating intracellular cholesterol accumulation. LXRs also exert balanced actions on inflammation in human macrophages, displaying both proinflammatory and anti-inflammatory effects.
methodsOur study explored the role of LXRs in the functional response of human macrophage to lipid-rich plaque environment. We used primary human macrophages treated with atheroma plaque extracts and assessed the impact of pharmacological LXR inhibition by GSK2033 on cholesterol homeostasis and inflammatory response. Ultimately, we evaluated macrophage and endothelial cell cross talk by assessing the impact of macrophage-conditioned supernatants on the human endothelial cell.
resultsLXR inhibition by GSK2033 resulted in increased levels of cholesterol and oxysterols in human macrophages, alongside notable changes in the cholesterol ester profile. This was accompanied by heightened secretion of proinflammatory cytokines such as IL (interleukin)-6 and TNFα (tumor necrosis factor-α), despite a transcriptional repression of IL-1β. Conditioned media from GSK2033-treated macrophages more effectively activated ICAM-1 (intercellular adhesion molecule-1) and CCL2 (C-C motif ligand 2) expression in endothelial cells.
conclusionsOur findings illustrate the intricate relationship between LXR function, cholesterol metabolism, and inflammation in human macrophages. While LXR is required for the proper handling of plaque lipids by macrophages, the differential regulation of IL-1β versus IL-6/TNFα secretion by LXRs could be challenging for potential pharmacological interventions.
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