We studied the effects of inulin on lipid metabolism with a model of atherosclerosis in LDL receptor-deficient mice using lipidomics and transcriptomics.
We generated myeloid cell-specific Ncor1 knockout mice and crossbred them with low-density lipoprotein receptor (Ldlr) knockouts to study the role of macrophage NCOR1 in atherosclerosis.
The History of the WHHL Rabbit, an Animal Model of Familial Hypercholesterolemia (II) - Contribution to the Development and Validation of the Therapeutics for Hypercholesterolemia and Atherosclerosis.
Familial hypercholesterolemia (FH) is a frequent genetic disorder characterized by elevated low-density lipoprotein (LDL)-cholesterol (LDL-C) levels and early onset of atherosclerotic cardiovascular disease.
In addition, pharmacological inhibition of ACLY by bempedoic acid, prevents dyslipidemia and attenuates atherosclerosis in hypercholesterolemic ApoE<sup>-/-</sup> mice, LDLr<sup>-/-</sup> mice, and LDLr<sup>-/-</sup> miniature pigs.
In conclusion, our study demonstrates that combination of MEK1/2 inhibitor and LXR ligand can synergistically reduce atherosclerosis in LDLR deficient mice without lipogenic side effects.
The aim of this study was to further investigate the relation between dietary choline and atherosclerosis in 2 atherogenic mouse models, the LDL receptor knockout (Ldlr-/-) and Apoe-/- mice.
Using bone marrow transplantation of LDL receptor knockout mice with TLR4KO bone marrow, we show that deficiency of TLR4 protects macrophages from lipid accumulation during atherosclerosis.
<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.
Since macrophages are vital players in nonalcoholic steatohepatitis (NASH) and atherosclerosis, we assessed the effect of ASMase inhibition on NASH and atherosclerosis cooperatively induced by high PA-containing high-fat diet (HP-HFD) and LPS in LDL receptor-deficient (LDLR-/-) mice.
Loss of 2 Akt (Protein Kinase B) Isoforms in Hematopoietic Cells Diminished Monocyte and Macrophage Survival and Reduces Atherosclerosis in Ldl Receptor-Null Mice.
LDLR KO along with LDLR/apoE double KO rabbits should provide a novel means for translational investigations of human hyperlipidemia and atherosclerosis.
Familial hypercholesterolemia (FH) is a monogenic disease characterized by high levels of low-density lipoprotein cholesterol and premature atherosclerotic cardiovascular disease.
In addition to being able to cross the endothelial barrier to become accumulated in subendothelial space and thereby initiate atherosclerosis, LDL may exert a direct effect on vascular endothelial cells through activation of LDL receptor and its downstream signaling.
An interspecies study of lipid profiles and atherosclerosis in familial hypercholesterolemia animal models with low-density lipoprotein receptor deficiency.
3-Hydroxyanthralinic acid Metabolism Controls the Hepatic Srebp/Lipoprotein axis, Inhibits Inflammasome Activation in Macrophages, and Decreases Atherosclerosis in LDLR-/- Mice.
Our findings demonstrate that, unlike other rodent animals, the levels of plasma cholesterol in hamsters can be significantly modulated by the intervention of dietary cholesterol, which were closely associated with severity of atherosclerosis in LDLR+/- hamsters, suggesting that the LDLR+/- hamster is an ideal animal model for FH and has great potential in the study of FH and atherosclerosis-related CHD.
The objective of this study is to examine the effects of NKT cell on lipid metabolism and the initiation and progression of atherosclerosis in LDL receptor deficient (LDLR<sup>-/-</sup>) mice.
In this study, we investigated the frequency of IL-10<sup>+</sup> B cells during the development of atherosclerosis in low-density lipoprotein receptor-deficient (Ldlr<sup>-/-</sup>) mice and studied the effect of adoptive transfer of IL-10<sup>+</sup> B cells on atherosclerosis.
Mutations in PCSK9 that strengthen its interactions with LDLR result in familial hypercholesterolemia (FH) and early onset atherosclerosis, while nonsense mutations of PCSK9 result in cardio-protective hypocholesterolemia.
The purpose of the present study was to investigate the possible effect of oral magnesium sulfate (MgSO<sub>4</sub> ) in the reduction of atherosclerosis plaques through inhibition of lectin-like low-density lipoprotein receptor-1 (LOX-1) gene expression in diabetic vessels.
Our findings suggest that despite improving adiposity and plasma triglycerides, pharmacologic activation of thermogenic adipocytes is not able to reverse atherosclerosis in LDLR-deficient mice.
Familial hypercholesterolemia (FH) is a common hereditary lipid disorder associated with substantial risk of premature atherosclerotic cardiovascular disease.