SIM is a BCL11a inhibitor and ROM is a HDAC inhibitor and both of these drugs are Food and Drug Administration (FDA)-approved for hypercholesterolemia and cutaneous T-cell lymphoma respectively.
Collectively, these results indicate that hypercholesterolemia per se is characterized by a resistance to GLP-1 effects on platelets and this impairment is not corrected by treatment with simvastatin.
In the recessive model, the carriers of the SLC15A1rs4646234 CC genotype showed a significantly reduced risk of hypercholesterolaemia (OR = 2.29, 95% CI = 1.23-4.28, P = .009).
Moreover, blocking FSH signaling by anti-FSHβ antibody or ablating the FSH receptor (FSHR) gene could effectively prevent hypercholesterolemia induced by FSH injection or high-cholesterol diet feeding.
Hypercholesterolemia is associated with reduced expression of miR-146b, which increases TRAF6-dependent inflammation and is associated with poor neovascularization in response to ischemia.
The impact of a high cholesterol diet (HCD) on the protein YWHAZ (14-3-3 ζ or tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein Zeta) was also investigated in our model.
The intake of the HC diet was associated with a higher level of lipid peroxidation (malondialdehyde, MDA) and a lower concentration of hepatic antioxidant enzymes (SOD, GPx, and GST), and all these factors were partially improved in the low-dose and high-dose HC + HO groups.
The rs1004467 and rs11191548 in the CYP17A1 gene are associated with a decreased risk of hypercholesterolemia and lower serum TC levels in Han Chinese.
The high CHO patients were subgrouped based on the computed tomography angiography results, that is, CHO+ no ART (n = 10), CHO+ ART less than 50% (n = 13), CHO+ ART 50-75% (n = 11), and CHO+ ART more than 75% (n = 6).
Hypercholesterolemia induces changes in the miRNA content of HDL enhancing miR126 and its delivery to endothelial cells with the consequent downregulation of its target gene HIF1α.
Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4α transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia.
In a mouse model combining hyperglycaemia and hypercholesterolaemia (streptozotocin diabetic, ApoE<sup>-/-</sup> mice), mice showed severe insulin resistance, renal dysfunction, micro-inflammation, subsequent extracellular matrix expansion and decreased expression of PTPN2.
SIM is a BCL11a inhibitor and ROM is a HDAC inhibitor and both of these drugs are Food and Drug Administration (FDA)-approved for hypercholesterolemia and cutaneous T-cell lymphoma respectively.
The dual phenotypes of progressive HL and hypercholesterolaemia resembled in OSBPL2-disrupted pigs confirmed the implication of OSBPL2 mutation in nonsydromic hearing loss (NSHL) and contributed to the potential linkage between auditory dysfunction and dyslipidaemia/hypercholesterolaemia.
High-cholesterol diet (HCD)-fed Mir652<sup>-/-</sup>Apoe<sup>-/-</sup> (Mir652<sup>-/-</sup>) mice and matching Mir652<sup>+/+</sup>Apoe<sup>-/-</sup> (Mir652<sup>+/+</sup>) mice were subjected to carotid injury to analyze the effects of miR-652 knockdown on endothelial repair.
Fibrosing steatohepatitis was established in Alms1 mutant (foz/foz) and C57BL/6J wildtype mice fed high-fat/high-cholesterol or methionine- and choline-deficient diet.
The associations among DHCR7, vitamin D and lipid profile followed a seasonal pattern, decreased DHCR7 (p = 0.008) and vitamin D (p < 0.001) and increased total-cholesterol (p = 0.025) being found in winter/spring.
These findings indicate that while endogenous SUMO2 is important in maintenance of normal endothelium-dependent vascular function, its upregulation impairs vascular homeostasis and contributes to hypercholesterolemia-induced endothelial dysfunction.<b>NEW & NOTEWORTHY</b> Sumoylation is known to impair vascular function; however, the role of specific SUMOs in the regulation of vascular function is not known.
Our results shed light into the mechanisms behind the cholesterol- and lipid-lowering effects of Pu-erh tea, and suggest that decreased intestinal BSH microbes and/or decreased FXR-FGF15 signaling may be potential anti-hypercholesterolemia and anti-hyperlipidemia therapies.
The high CHO patients were subgrouped based on the computed tomography angiography results, that is, CHO+ no ART (n = 10), CHO+ ART less than 50% (n = 13), CHO+ ART 50-75% (n = 11), and CHO+ ART more than 75% (n = 6).
Hp2-2 and Hp0 collectively was strongly associated with hypertension (OR = 2.54, P = 0.011), obesity (OR = 5.97, P < 0.001) and hypercholesterolaemia (OR = 2.99, P < 0.001).
We hypothesized that hypercholesterolemia could affect vascular repair processes and promote post-transplant renal vascular remodeling through the over-expression of the anti-angiogenic thrombospondin-1 interacting with vascular endothelial growth factor-A levels.
In addition, we found that policosanol supplementation stimulated an increase in fecal cholesterol and bile acid contents and deactivated 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase by AMP-activated protein kinase (AMPK) phosphorylation during high-fat and high-cholesterol-containing diet-induced development of hypercholesterolemia.