<b>Background and Aim:</b> Previously, we found that short chain fatty acids (SCFA) inhibit LPS or TNFα-induced endothelial inflammatory responses and excessive vascular cell adhesion molecule-1 (VCAM-1) expression, two important steps in the development of atherosclerosis.
<b>Background:</b> Paraoxonase 1 (PON1: EC 3.1.8.1) is a vital antioxidant enzyme against mainly atherosclerosis and many other diseases associated with oxidative stress.
<b>Background:</b> Tumour necrosis factor like cytokine 1A (TL1A), which is a member of tumour necrosis factor alpha superfamily (TNF-α), is a novel indicator of atherosclerosis.<b>Objective:</b> Smoking is an established stimulant of TNF-α.
<b>Conclusion:</b> Exosomal miR-21-3p from nicotine-treated macrophages may accelerate the development of atherosclerosis by increasing VSMC migration and proliferation through its target PTEN.
<b>Conclusion:</b> These results indicate that CUMS exacerbates atherosclerosis is likely via HMGB1-mediated downregulation of PPARγ/LXRα-ABCA1 through TLR4.
<b>Conclusions:</b> Our work shows that <i>in vivo</i> AAV-CRISPR/Cas9-mediated <i>Ldlr</i> gene correction can partially rescue LDLR expression and effectively ameliorate atherosclerosis phenotypes in <i>Ldlr</i> mutants, providing a potential therapeutic approach for the treatment of FH patients.
<b>Methods</b>: Pubmed and Embase were searched to identify studies which estimated the effect of isolated alkaloids on atherosclerosis in apolipoprotein E deficient mice.
<b>Methods</b>: We induced experimental atherosclerosis in ApoE<sup>-/-</sup>IRF1<sup>-/-</sup> mice and evaluated the effect of IRF1 on disease progression and foam cell formation.
<b>Methods:</b> Apolipoprotein E-deficient (Apoe<sup>-/-</sup>) mice fed a high-fat diet were given intraperitoneal injections of SAP (6 mg/kg) every other day for a total of 2 weeks to characterize atherosclerosis development.
<b>Objective:</b> AIP1 expression is downregulated in human atherosclerotic plaques and global deletion of AIP1 in mice exacerbates atherosclerosis in ApoE-KO mouse models.
<b>Objective:</b> AIP1 expression is downregulated in human atherosclerotic plaques and global deletion of AIP1 in mice exacerbates atherosclerosis in ApoE-KO mouse models.
<b>Objective:</b> AIP1 expression is downregulated in human atherosclerotic plaques and global deletion of AIP1 in mice exacerbates atherosclerosis in ApoE-KO mouse models.