2018
DOI: 10.1016/j.biopha.2017.11.016
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Trimethylamine N-oxide promotes atherosclerosis via CD36-dependent MAPK/JNK pathway

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Cited by 231 publications
(169 citation statements)
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References 28 publications
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“…Besides, TMAO was reported to up-regulate the expression of macrophage receptors (CD36 and SR-A1) in ApoE −/− mice fed a high-choline or high-TMAO diet (Wang et al 2011), as well as in TMAO-treated murine macrophage J774A.1 cells (Mohammadi et al 2016), facilitating the up-take of cholesterol into macrophage and foam cell formation. Subsequently, Geng et al (2017) observed accelerated atherosclerotic plaque progression, promoted macrophage recruitment, higher CD36 and pro-inflammatory cytokine expression in the plaque lesions in high-TMAO-fed ApoE −/− mice. They also found that TMAO-related foam cell formation was mediated, at least partially, by the CD36/MAPK/JNK pathway (Geng et al 2017).…”
Section: Tmao-induced Endothelial Dysfunctionmentioning
confidence: 85%
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“…Besides, TMAO was reported to up-regulate the expression of macrophage receptors (CD36 and SR-A1) in ApoE −/− mice fed a high-choline or high-TMAO diet (Wang et al 2011), as well as in TMAO-treated murine macrophage J774A.1 cells (Mohammadi et al 2016), facilitating the up-take of cholesterol into macrophage and foam cell formation. Subsequently, Geng et al (2017) observed accelerated atherosclerotic plaque progression, promoted macrophage recruitment, higher CD36 and pro-inflammatory cytokine expression in the plaque lesions in high-TMAO-fed ApoE −/− mice. They also found that TMAO-related foam cell formation was mediated, at least partially, by the CD36/MAPK/JNK pathway (Geng et al 2017).…”
Section: Tmao-induced Endothelial Dysfunctionmentioning
confidence: 85%
“…Subsequently, Geng et al (2017) observed accelerated atherosclerotic plaque progression, promoted macrophage recruitment, higher CD36 and pro-inflammatory cytokine expression in the plaque lesions in high-TMAO-fed ApoE −/− mice. They also found that TMAO-related foam cell formation was mediated, at least partially, by the CD36/MAPK/JNK pathway (Geng et al 2017). However, in murine J447 macrophage treated with acetylated-LDL, TMAO in increasing concentrations did not alter the cholesterol uptake or efflux (Collins et al 2016).…”
Section: Tmao-induced Endothelial Dysfunctionmentioning
confidence: 85%
See 1 more Smart Citation
“…After differentiation from monocytes initially, macrophages can sense and intake the oxidized modified LDLs (ox‐LDL) by the action of cluster of differentiation 36(CD36) and class A1 scavenger receptors (SR‐A1), which are the macrophage scavenger receptors (SRs) with high affinity to sense ox‐LDL (). TMAO plays an important role in augmenting the accumulation of ox‐LDL within macrophages by upregulating the expression of CD36 and SR‐A1 (). In this process, more macrophage cells are transformed into foam cells.…”
Section: Foam Cells Formationmentioning
confidence: 99%
“…TMA, a by-product of the bacterial metabolism of carnitine, choline, and other and choline-containing compounds, is absorbed by the host and transformed in the liver into trimethylamine N-oxide (TMAO) (15). In turn, circulating TMAO inhibits cholesterol transport and promotes its accumulation in macrophages, inducing the formation of artherosclerotic plaques (16). Decreasing TMA levels in the gut, and reducing circulating TMAO levels, has been proposed as a therapeutic strategy for cardiovascular disease (17).…”
Section: Introductionmentioning
confidence: 99%