<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.
<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>Results and disccussion:</b> G31P suppressed the abnormal lipid profile and decreased the levels of KC, MMP-2, MMP-9, PCNA, and Mef2a in a mouse model of atherosclerosis.
<b>Results:</b> MiR-25-3p was expressed poorly in ox-LDL-induced CVECs and vascular tissues but exhibited high levels of expression in thrombin-induced PLT-Exo of atherosclerosis models of ApoE<sup>-/-</sup> mice.
<b>Results:</b> Our results indicated that the protein levels of HMGB1, TLR4, and pro-inflammatory cytokines including IL-1β, TNF-α were elevated with the development of atherosclerosis in CUMS mice, while the expressions of PPARγ, LXRα, and ABCA1 declined.
<b>Results:</b> Our results indicated that the protein levels of HMGB1, TLR4, and pro-inflammatory cytokines including IL-1β, TNF-α were elevated with the development of atherosclerosis in CUMS mice, while the expressions of PPARγ, LXRα, and ABCA1 declined.
<b>Results:</b> Our results indicated that the protein levels of HMGB1, TLR4, and pro-inflammatory cytokines including IL-1β, TNF-α were elevated with the development of atherosclerosis in CUMS mice, while the expressions of PPARγ, LXRα, and ABCA1 declined.
<b>Results:</b> Our results indicated that the protein levels of HMGB1, TLR4, and pro-inflammatory cytokines including IL-1β, TNF-α were elevated with the development of atherosclerosis in CUMS mice, while the expressions of PPARγ, LXRα, and ABCA1 declined.
<b>Results:</b> Our results indicated that the protein levels of HMGB1, TLR4, and pro-inflammatory cytokines including IL-1β, TNF-α were elevated with the development of atherosclerosis in CUMS mice, while the expressions of PPARγ, LXRα, and ABCA1declined.
<b>Results:</b><i>In vivo</i> experiments confirmed that paeonol restricted atherosclerosis development and increased miR-223 expression, inhibited STAT3 pathway in ApoE<sup>-/-</sup> mice.
<i>ASPH</i>, through interaction with <i>CACNA2D4</i> (calcium voltage-gated channel auxiliary subunit alpha2delta 4), may be associated with atherosclerosis by regulating the cellular response to calcium ion; and <i>PDE3B</i> may exert roles in negative regulation of angiogenesis through cross talk with <i>ELMO1</i> (engulfment and cell motility 1).
<i>ASPH</i>, through interaction with <i>CACNA2D4</i> (calcium voltage-gated channel auxiliary subunit alpha2delta 4), may be associated with atherosclerosis by regulating the cellular response to calcium ion; and <i>PDE3B</i> may exert roles in negative regulation of angiogenesis through cross talk with <i>ELMO1</i> (engulfment and cell motility 1).
<i>Atg16l1</i> deletion in DCs (all CD11c-expressing cells) expands aortic regulatory T cells in vivo, limits the accumulation of T helper cells type 1, and reduces the development of atherosclerosis in <i>Ldlr</i><sup>-/-</sup> mice.
<i>Background</i>: The expression of matrix metalloproteinases 2/9 (MMP-2/9) has been implicated in arterial remodeling and inflammation in atherosclerosis.
<i>In vivo</i> experiments were performed in 2-mo-old atherosclerosis-prone apolipoprotein E-deficient/LDL receptor-deficient (ApoE<sup>-/-</sup>/LDLR<sup>-/-</sup>) female mice and their wild-type C57BL/6J littermates.
<i>In vivo</i> studies examining the role of SP-D in the development of atherosclerosis agree that SP-D plays a proatherogenic role, with SP-D knockout mice having smaller atherosclerotic plaque areas, which might be caused by a decreased systemic inflammation.
<i>SMAD3</i> and <i>NOP56</i>), and also hub proteins associated with metal-DMRs only but with relevant connections with atherosclerosis effectors (e.g.