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.
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.
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.
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.
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.
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.
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.
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.
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.
As Vav1 and Vav3 were found to exert function in atherosclerosis development, it remains thus to decipher whether Vav2 also plays a role in the development of atherosclerosis.
The aim of this study was to address whether KRIT1 loss-of-function predisposes to the development of pathological conditions associated with enhanced endothelial cell susceptibility to oxidative stress and inflammation, such as arterial endothelial dysfunction (ED) and 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.
Adherens junction protein p120 is thought to be crucial for maintaining vascular integrity, which is important in many pathologies and diseases including atherosclerosis, vascular malformations, hemorrhagic stroke, sepsis and others.
Whether the PRRs of the C-type lectin receptor (CLR) family including Dectin-2 may be involved in the pathogenesis of atherosclerosis remains largely unknown.
Collectively, these results suggested that miR‑140‑5p aggravated hypertension and oxidative stress of mice with atherosclerosis by targeting Nrf2 and Sirt2.
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.
The present review describes the histology and homeostasis of arteries by explaining EC function/dysfunction and discusses BMP-9 effect on EC behavior, considering factors engaged in the development of atherosclerosis.
After controlling for age, body mass index, population structure and cell composition, 26 epigenome-wide significant sites (FDR q < 0.05) were identified, including the AHRR and PHF14 genes associated with atherosclerosis and lung disease, respectively.