ArticleJournal of advanced research2024
The exoprotein Gbp of Fusobacterium nucleatum promotes THP-1 cell lipid deposition by binding to CypA and activating PI3K-AKT/MAPK/NF-κB pathways.
Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Diagnostic biomarkers for non-traumatic osteonecrosis of the femoral head : a systematic review and pathophysiological cascade network.Bone & joint research · 2026Pooled it
- Lipid Metabolic Reprogramming in Periodontitis-Associated Alveolar Bone Remodeling: Mechanisms, Signaling Pathways, and Therapeutic Implications.Biomolecules · 2026Review
- Article
- Lipopolysaccharide promotes rheumatoid arthritis by enhancing Wnt7b mediated macrophage-FLS communication.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Identification of circadian rhythm-associated key genes in metabolic dysfunction-associated fatty liver disease.Clinical and experimental medicine · 2026Article
- Decoding the Gut-Fat-Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies.International journal of molecular sciences · 2026Review
- Polystyrene nanoplastics and benzo(a)pyrene synergistically induce lung fibrosis and inflammation via relaxin signalling in mice.Communications biology · 2026Article
- A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury.Cell reports. Medicine · 2026Article
- Single-cell RNA-seq and in vitro study reveal Fusobacterium nucleatum impairs β-cell identity in type 2 diabetes via the NF-κB-CDKN1C axis.Journal of translational medicine · 2026Article
- Fusobacterium nucleatum: ecology, pathogenesis and clinical implications.Nature reviews. Microbiology · 2026Review
- Caspase Recruitment Domain Family Member 8: A Favorable Target in the Pathogenesis of Atherosclerosis.Reviews in cardiovascular medicine · 2026Review
- A temporally functional composite hydrogel scaffold for cranial defect repair via sequential modulation of angiogenesis and osteogenesis.Theranostics · 2026Article
- Deciphering the Multi-Target Therapeutic Mechanisms of Traditional Chinese Medicine Against Alzheimer's Disease: A Network Pharmacology Perspective.Drug design, development and therapy · 2026Review
- Fusobacterium nucleatum drives gastric cancer metastasis via Gbp-CypA-NF-κB-mediated CXCL8 crosstalk between tumor cells and mast cells.Cell communication and signaling : CCS · 2025Article
- Targeted suppression of CCR7/NF-κB signaling by apoptotic body-inspired colchicine nanovesicles halts atherosclerotic progression.Journal of nanobiotechnology · 2025Article
- Review
- CD160 dictates anti-PD-1 immunotherapy resistance by regulating CD8Nature cell biology · 2025Article
- Lipid accumulation inhibition strategies alleviate Fusobacterium nucleatum-infected colorectal cancer.Microbiome · 2025Article
- Myeloid-derived MANF ameliorates ethanol-induced liver injury by enhancing microRNA-223 expression.Journal of gastroenterology · 2025Article
- Porphyromonas gingivalis aggravates atherosclerotic plaque instability by promoting lipid-laden macrophage necroptosis.Signal transduction and targeted therapy · 2025Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionGrowing evidence has shown the correlation between periodontitis and atherosclerosis, while our knowledge on the pathogenesis of periodontitis-promoting atherosclerosis is far from sufficient.
objectivesIlluminate the pathogenic effects of Fusobacterium nucleatum (F. nucleatum) on intracellular lipid deposition in THP-1-derived macrophages and elucidate the underlying pathogenic mechanism of how F. nucleatum promoting atherosclerosis. METHODS AND
resultsF. nucleatum was frequently detected in different kinds of atherosclerotic plaques and its abundance was positively correlated with the proportion of macrophages. In vitro assays showed F. nucleatum could adhere to and invade THP-1 cells, and survive continuously in macrophages for 24 h. F. nucleatum stimulation alone could significantly promote cellular inflammation, lipid uptake and inhibit lipid outflow. The dynamic gene expression of THP-1 cells demonstrated that F. nucleatum could time-serially induce the over-expression of multiple inflammatory related genes and activate NF-κB, MAPK and PI3K-AKT signaling pathways. The exoprotein of F. nucleatum, D-galactose-binding protein (Gbp), acted as one of the main pathogenic proteins to interact with the Cyclophilin A (CypA) of THP-1 cells and induced the activation of the NF- κB, MAPK and PI3K-AKT signaling pathways. Furthermore, use of six candidate drugs targeting to the key proteins in NF- κB, MAPK and PI3K-AKT pathways could dramatically decrease F. nucleatum induced inflammation and lipid deposition in THP-1 cells.
conclusionsThis study suggests that the periodontal pathogen F. nucleatum can activate macrophage PI3K-AKT/MAPK/NF-κB signal pathways, promotes inflammation, enhances cholesterol uptake, reduces lipid excretion, and promotes lipid deposition, which may be one of its main strategies promoting the development of atherosclerosis.
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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 OpenQuestion graph.