ArticleFrontiers in cardiovascular medicine2022
Monocyte and Macrophage Lipid Accumulation Results in Down-Regulated Type-I Interferon Responses.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Lipid-Laden M1-like Macrophages of Familial Hypercholesterolemia Patients Are Characterized by Increased Interleukin-1β Secretion and ReducedCurrent issues in molecular biology · 2026Article
- Lipid deprivation amplifies type I IFN responses in monocytes through prenylation: insights from familial combined hypolipidemia type 2.Journal of translational medicine · 2025Article
- Downregulation of type I interferon signalling pathway by urate in primary human PBMCs.Immunology · 2025Article
- In Silico Analysis Revealed Marco (SR-A6) and Abca1/2 as Potential Regulators of Lipid Metabolism in M1 Macrophage Hysteresis.International journal of molecular sciences · 2024Article
- Cholesterol overload in macrophages drives metabolic dysfunction-associated steatohepatitis via inhibiting 7-dehydrocholesterol reductase in mice.Journal of translational medicine · 2024Article
- Examining Chronic Inflammation, Immune Metabolism, and T Cell Dysfunction in HIV Infection.Viruses · 2024Review
- Article
- Multi-omics computational analysis unveils the involvement of AP-1 and CTCF in hysteresis of chromatin states during macrophage polarization.Frontiers in immunology · 2023Article
- Alterations in the Kynurenine-Tryptophan Pathway and Lipid Dysregulation Are Preserved Features of COVID-19 in Hemodialysis.International journal of molecular sciences · 2022Article
- Commentary: Monocyte and macrophage lipid accumulation results in down-regulated type-I interferon responses.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are critical components of atherosclerotic lesions and their pro- and anti-inflammatory responses influence atherogenesis. Type-I interferons (IFNs) are cytokines that play an essential role in antiviral responses and inflammatory activation and have been shown to promote atherosclerosis. Although the impact of type-I IFNs on macrophage foam cell formation is well-documented, the effect of lipid accumulation in monocytes and macrophages on type-I IFN responses remains unknown. Here we examined IFN stimulated (ISG) and non-ISG inflammatory gene expression in mouse and human macrophages that were loaded with acetylated LDL (acLDL), as a model for foam cell formation. We found that acLDL loading in mouse and human macrophages specifically suppressed expression of ISGs and IFN-β secretion, but not other pro-inflammatory genes. The down regulation of ISGs could be rescued by exogenous IFN-β supplementation. Activation of the cholesterol-sensing nuclear liver X receptor (LXR) recapitulated the cholesterol-initiated type-I IFN suppression. Additional analyses of murine
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