ArticleCell biology and toxicology2023
TRIM64 promotes ox-LDL-induced foam cell formation, pyroptosis, and inflammation in THP-1-derived macrophages by activating a feedback loop with NF-κB via IκBα ubiquitination.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 14 citations in OpenAlex.
- The ubiquitin system in heart and vessel pathobiology: From mechanisms to therapeutic strategies.Genes & diseases · 2026Review
- Daidzein Mitigates Nicotine-Induced Atherogenesis via Nrf2/ROS/TXNIP-Dependent Inhibition of Macrophage Pyroptosis and Lipid Accumulation.Molecular nutrition & food research · 2026Article
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Foam Cells: The Origin of Formation and Target for Plant-derived Bioactive Compounds.Current medicinal chemistry · 2026Review
- Delving into pyroptosis in atherosclerosis: role, mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Enrichment of the TRIM21-IgG complex in placental villi during HIV-1 infection.Frontiers in immunology · 2026Article
- FBXL8 Stabilizes IκBα and Negatively Regulated NF-κB Activation to Suppress Pancreatic Cancer Progression.International journal of biological sciences · 2026Article
- Monocytes/Macrophages and Atherogenesis.International journal of molecular sciences · 2025Review
- FBXO22 Suppresses Oxidative Stress-Induced ASK1 Activation and Cell Death via Ubiquitination-Dependent Degradation of TRIM48.International journal of molecular sciences · 2025Article
- Vitamin D immune modulation of the anti-inflammatory effects of HDL-associated proteins.Lipids in health and disease · 2025Review
- Insights from human NF-κB knockouts.EMBO reports · 2025Review
- The Role of Ubiquitination on Macrophages in Cardiovascular Diseases and Targeted Treatment.International journal of molecular sciences · 2025Review
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Macrophage pyroptosis in atherosclerosis: therapeutic potential.Acta biochimica et biophysica Sinica · 2025Review
- Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.Frontiers in immunology · 2025Article
- Inflammation in atherosclerosis: pathophysiology and mechanisms.Cell death & disease · 2024Review
- Ubiquitous regulation of cerebrovascular diseases by ubiquitin-modifying enzymes.Clinical and translational medicine · 2024Review
- Genetic Association Analysis of Copy Number Variations for Meat Quality in Beef Cattle.Foods (Basel, Switzerland) · 2023Article
- Anti-inflammatory Pathways of Novel Anti-diabetic Therapies. A Literature Review.In vivo (Athens, Greece)Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a chronic inflammatory disease and the main pathology behind most cardiovascular diseases and the overactivation of macrophages initiates the development of atherosclerosis. However, the specific functions of oxidized low-density lipoprotein (ox-LDL) in macrophages remain elusive. Macrophages derived from monocyte (THP-1) were treated with ox-LDL and were used to generate atherosclerosis in an in vitro model. NLRP3 inflammasome markers were examined using quantitative RT-PCR and Western blotting. Cytokines were measured using ELISA. Chromatin immunoprecipitation (ChIP) was utilized to detect nuclear factor kappa B (NF-κB) and TRIM64 interactions. A fat-rich diet was applied to ApoE-/- mice for in vivo studies. ox-LDL promoted TRIM64 expression in a time-dependent manner. According to loss- and gain-of-function analyses, TRIM64 enhanced the activation of NLRP3 inflammasomes and the expression of downstream molecules. TRIM64 directly interacted with IκBα and promoted IκBα ubiquitination at K67 to activate NF-κB signaling. We detected direct binding between NF-κB and the TRIM64 promoter, as well as enhanced TRIM64 expression. Our study revealed an interaction between TRIM64 and NF-κB in the development of atherosclerosis. TRIM64 and NF-κB formed a positive feedback to activate NF-κB pathway. ox-LDL induces foam cell formation and TRIM64 expression TRIM64 regulates ox-LDL-induced foam cell formation, pyroptosis and inflammation via the NF-κB signaling TRIM64 activates NF-κB signaling by ubiquitination of IκBα NF-κB inhibition attenuates atherosclerosis in HFD-induced ApoE (-/-) mice.
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