Although RCe1 was significantly higher than RCe2, non-fasting RCe, no matter RCe1 or RCe2, after a daily breakfast was an independent predictor for CHD risk in Chinese subjects, indicating that the non-fasting state is critical in the development of atherosclerosis.
Thus, we concluded that inhibition of SCARB1 expression induced by DNMT3b at least partly accelerated Hcy-mediated atherosclerosis through promoting lipid accumulation in foam cells, which was attributed to the decreased binding of SP1 to SCARB1 promoter.
Main pre-specified secondary outcomes included changes in FBS subcomponents and the impact of the knowledge of presence of atherosclerosis as assessed by bilateral carotid/femoral vascular ultrasound.
The obtained data suggest that high levels of circulating resistin acting upon cells with an upregulated CAP1 gene could contribute to the increased inflammation and accelerated atherosclerosis seen in CKD patients.
We revealed for the first time that miR-217-5p inhibited apoptosis of endothelial cells in atherosclerosis and identified CLIC4 as a novel target of miR-217-5p.
The four and a half LIM domain protein 2 (FHL2) is a member of the four and a half LIM domain (FHL) gene family, and it is associated with cholesterol-enriched diet-promoted atherosclerosis.
Elderly patients with AD (>60 years old) exhibited striking upregulation of key proinflammatory proteins, including markers of atherosclerosis (CCL4, CCL7, SORT1), cardiovascular risk (GDF15, MPO, ST2), cell adhesion (CDH3), and apoptosis (FAS; all P < .05) compared with younger patients with AD and age-matched controls.
Importantly, ApoE<sup>-</sup><sup>/</sup><sup>-</sup> mice injected with TIPE1 recombinant lentivirus developed significantly severe atherosclerosis accompanied by hyperglycemia, hypercholesterolemia and increased white blood count.
CCAAT/enhancer-binding protein beta (C/EBPβ) is a transcription factor, and its inhibition has recently been shown to prevent atherosclerosis development and foam cell formation.
Moreover, patients that were taking atorvastatin, had 1.5 (<i>p</i> = 0.04) times higher hsa-miR-24-3p expression in blood plasma.<b>Conclusions.</b> Our data suggest that hsa-miR-24-3p might have an effect on CYP4F2 activity during atherosclerosis.
Main pre-specified secondary outcomes included changes in FBS subcomponents and the impact of the knowledge of presence of atherosclerosis as assessed by bilateral carotid/femoral vascular ultrasound.
Contrary to our hypothesis, hA rg neither inhibited TNAP activity in vivo nor reduced coronary artery calcification and atherosclerosis in WHC -endothelial TNAP mice; however, compared with the placebo, hA rg prevented left ventricular dilatation ( P<0.01), preserved ejection fraction ( P<0.05), and reduced myocardial fibrosis ( P<0.001).
Transcription factor (TF) binding motif analysis within RE sequences identified over-representation of ETS, Zinc finger, and activator protein 1 TF families that regulate cell cycle, proliferation, and apoptosis, implicating them in the development of atherosclerosis.
These results indicate that serum OPN levels were strongly associated with subclinical atherosclerosis in patients with LES and it might be a useful CV biomarker that requires additional validation in larger trials.
Our previous study revealed that Homeobox containing 1 (HMBOX1), essential for the survival of vascular endothelial cells (VECs), was involved in the progression of atherosclerosis.
We used transparent transgenic zebrafish larvae Tg(lysc:EGFP), Tg(mpx:EGFP), Tg(mpeg1:EGFP), Tg(flk1:EGFP) or Tg(lysc:EGFP/flk1:mCherry), together with fluorescently labeled control and high cholesterol diets (HCD), to dynamically investigate the early development of atherosclerosis with confocal in vivo.
Here we use mouse models of atherosclerosis-a major underlying cause of mortality worldwide-to demonstrate that extracellular histone H4-mediated membrane lysis of smooth muscle cells (SMCs) triggers arterial tissue damage and inflammation.