2018
DOI: 10.1016/j.bbrc.2017.11.025
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Inhibition of the NLRP3 inflammasome attenuates foam cell formation of THP-1 macrophages by suppressing ox-LDL uptake and promoting cholesterol efflux

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Cited by 40 publications
(29 citation statements)
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“…Therefore, we suggested that promotion of NLRP3 inflammasome will harm process of cholesterol efflux. This is similar to conclusion by Chen et al 50 According to Chen et al, inhibition of the NLRP3 inflammasome decreases foam cell formation of THP-1 macrophages via suppression of ox-LDL uptake and enhancement of cholesterol efflux. However, report also suggests that Cholesterol accumulation in myeloid cells activates the NLRP3 inflammasome, which enhances neutrophil accumulation and neutrophil extracellular trap formation in atherosclerotic plaques, and promotion of cholesterol efflux suppress inflammasome activation.…”
Section: Discussionsupporting
confidence: 91%
“…Therefore, we suggested that promotion of NLRP3 inflammasome will harm process of cholesterol efflux. This is similar to conclusion by Chen et al 50 According to Chen et al, inhibition of the NLRP3 inflammasome decreases foam cell formation of THP-1 macrophages via suppression of ox-LDL uptake and enhancement of cholesterol efflux. However, report also suggests that Cholesterol accumulation in myeloid cells activates the NLRP3 inflammasome, which enhances neutrophil accumulation and neutrophil extracellular trap formation in atherosclerotic plaques, and promotion of cholesterol efflux suppress inflammasome activation.…”
Section: Discussionsupporting
confidence: 91%
“…Indeed, selectively inhibiting Nlrp3 restricts oxLDL uptake by THP-1 MOs, thus impairing foam cell formation. This inhibition also led to the downregulation of Cd36, which, in the context of the findings by Sheedy et al ( 2013 ), almost certainly limited the appearance of foam cells (Chen et al, 2018 ). Several recent reviews have also focussed on NLRP3 as nexus between oxidized lipids and inflammatory cytokine release in atherosclerosis (Baldrighi et al, 2017 ; Patel et al, 2017 ; Hoseini et al, 2018 ).…”
Section: A Broad Spectrum Of Lipid and Lipoprotein Species Modulate Imentioning
confidence: 71%
“…The CD36 gene transcription is regulated by peroxisome proliferator-activated receptor-g (PPARg) (Nagy et al, 1998;Tontonoz et al, 1998), nuclear erythroid-related factor 2 (Nrf2) (Ishii et al, 2004;Olagnier et al, 2011), as well as by signal transducer and activator of transcription 1 (STAT1) (Kotla et al, 2017) pathways. In addition, CD36 expression can also be regulated by retinol-binding protein 4 (Liu et al, 2017b), protein kinase Cu (PKCu)/activating transcription factor 2 (Raghavan et al, 2018), epidermal growth factor receptor (Zeboudj et al, 2018), trimethylamine N-oxide (Geng et al, 2018), NACHT, LRR, and PYD domains-containing protein 3 inflammasome (Chen et al, 2018b), transient receptor potential vanilloid 4 (TRPV4) (Goswami et al, 2017), cellular communication network factor 3 (Shi et al, 2017), melanocortin 1 receptor (Rinne et al, 2017), cluster of differentiation 146 (CD146) (Luo et al, 2017), triggering receptor expressed on myeloid cells (Joffre et al, 2016), cyclophilin A (Ramachandran et al, 2016), and many others. Furthermore, CD36-mediated foam cell formation and atherosclerosis were negatively regulated by C1q/tumor necrosis factor-related protein 13 via autophagy/lysosomedependent degradation of CD36 (Wang et al, 2019a).…”
Section: A Cholesterol Uptakementioning
confidence: 99%
“…Recently, Shibuya et al (2018) identified a highly potent ACAT1 inhibitor (IC 50 5 4.0 nM), which reduced lipid-accumulation in the aortic arch of hamsters fed with an atherogenic diet, raising the therapeutic potential of this compound to attenuate atherosclerosis in other experimental animal models and human patients with atherosclerosis. Other recent studies have shown that other treatment options, such as losartan (Rafatian et al, 2013) or inhibition of the NLRP3 inflammasome (by compound MCC950) (Chen et al, 2018b), inhibit the ACAT activity, CE accumulation, and foam cell formation. However, three randomized, double-blind, placebo-controlled trials failed to observe significant differences in carotid as well as coronary atherosclerosis between treatment with ACAT inhibitors (by pactimibe and avasimibe) and placebo (Tardif et al, 2004;Nissen et al, 2006;Meuwese et al, 2009).…”
Section: B Cholesterol Esterification and Hydrolysismentioning
confidence: 99%