2024
DOI: 10.1016/j.jare.2023.04.007
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The exoprotein Gbp of Fusobacterium nucleatum promotes THP-1 cell lipid deposition by binding to CypA and activating PI3K-AKT/MAPK/NF-κB pathways

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Cited by 13 publications
(6 citation statements)
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“…Noteworthy is the fact that many of the pro-tumor activities of P. gingivalis and F. nucleatum depend on the capability that the two bacteria have to activate the PI3K/AKT intracellular signaling pathway that is key to OSCC development and progression [39,47,189].…”
Section: Discussionmentioning
confidence: 99%
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“…Noteworthy is the fact that many of the pro-tumor activities of P. gingivalis and F. nucleatum depend on the capability that the two bacteria have to activate the PI3K/AKT intracellular signaling pathway that is key to OSCC development and progression [39,47,189].…”
Section: Discussionmentioning
confidence: 99%
“…Consequently, circulating OSCC cells may undergo a peculiar, fast-occurring type of apoptosis that is termed "anoikis" [107]. In this regard, the activation of the PI3K/AKT signaling pathway promoted by P. gingivalis [39] or F. nucleatum [47] makes OSCC cells resistant to anoikis [107], thereby effectively favoring OSCC metastasization.…”
Section: Effects Of P Gingivalis and F Nucleatum Leading To Oscc Prog...mentioning
confidence: 99%
“…Studies have demonstrated that microbial species can be transmitted from the oral cavity to the gut and that the oral and gut microbiota can interact with each other 11 . Given the association between dental health and both endothelial dysfunction and atherosclerotic disease, the gut may serve as a niche or entry path for hematogenous spread of bacteria that are pathogenic in the oral cavity 36 , 37 . These studies suggest that bacteria in the oral cavity are associated with cardiovascular disease and may spread to the circulation to affect the growth and stability of atherosclerotic plaques.…”
Section: Gut Microbiome In the Onset And Progression Of Atherosclerosismentioning
confidence: 99%
“…Fn fosters hepatic glycolysis and lipid synthesis through the PI3K/Akt/mTOR signaling pathway, thus uplifting plasma lipid concentrations and exacerbating AS in mice [ 150 ]. Fn -infected macrophages exhibit an activation of the PI3K-AKT/MAPK/NF-κB signaling pathway, propelling the inflammatory responses and cholesterol uptake, concurrently reducing lipid excretion, leading to lipid deposition [ 156 ]. Another study revealed that Fn stimulates macrophages to undergo abnormal pro-inflammatory responses, M1 polarization, and cell apoptosis, triggering the release of inflammatory cytokines such as IL-6, IL-1β, IL-17, and TNF-α.…”
Section: Fusobacterium Nucleatummentioning
confidence: 99%
“…In addition, Fn upregulates FABP4 via a JNK-dependent mechanism in macrophages, thereby augmenting lipid uptake by macrophages [98] (Figure 3) (Table 3). Increased plasma TG and cholesterol levels [150,151]; elevated serum levels of IL-6, CRP, and LDL, decreased levels of HDL [152] A positivity rate of 34% in carotid endarterectomy specimens [147]; ruptured cerebral aneurysms [120]; stable CAD [149] Upregulated chemotactic factors and cell adhesion molecules [152] Hepatic cells Glycolysis and lipid synthesis PI3K/Akt/mTOR signaling pathway [150] Monocytes Inflammatory responses PI3K-AKT/MAPK/NF-κB signaling pathway [156] M1 polarization; cell apoptosis cholesterol accumulation modulation of lipid metabolism-related genes including SR-A1, ACAT-1, ABCA1 and ABCG1 [151]; upregulation of FABP4 via a JNK-dependent mechanism [98]…”
Section: Mechanistic Investigations On the Effect Of Fn In Asmentioning
confidence: 99%