Familial hypercholesterolemia (FH) is a severe genetic hyperlipidemia characterized by increased levels of low-density lipoprotein cholesterol (LDL-C), leading to premature atherosclerosis.
Here, we show that the autophagic flux in atherosclerosis-susceptible <i>Ldlr</i><sup>-/-</sup> (low-density lipoprotein receptor-deficient) mice is substantially higher in splenic and aortic DCs compared with macrophages and is further activated under hypercholesterolemic conditions.
Rosuvastatin significantly reduced plasma cholesterol in hypercholesterolemic mice in the absence of LDLR but had no effects on atherosclerosis at aortic sinus level or in coronary arteries.
Familial Hypercholesterolemia (FH) is a genetic condition that predisposes patients to substantially increased risk of early-onset atherosclerotic cardiovascular disease.
The low-density lipoprotein receptor-deficient (Ldlr<sup>-/-</sup>) mouse has been utilized by cardiovascular researchers for more than two decades to study atherosclerosis.
Familial hypercholesterolemia is an Mendelian dominant disorder characterized by defects of the low density lipoprotein receptor (LDLR) that result in a defective removal of LDL from plasma, which promotes deposition of cholesterol in the skin (xanthelasma), tendons (xanthomas), and arteries (atherosclerosis).
Conclusions These data demonstrate that adipocyte IKK β signaling affects the evolution of atherosclerosis plaque vulnerability in obese LDLR <sup>-/-</sup> mice.
In the remaining mice, plasma cholesterol was lowered by switching to chow diet and treatment with LDLR sense oligonucleotides to induce atherosclerosis regression.
Atherosclerosis in vivo was studied by transplanting bone marrow from male Flna <sup>o/fl</sup>/ LC mice to atherogenic low-density lipoprotein receptor-deficient ( Ldlr<sup>-/-</sup>) mice; and by infecting Flna <sup>o/fl</sup> and Flna <sup>o/fl</sup>/ LC mice with AdPCSK9 (adenoviral vector overexpressing proprotein convertase subtilisin/kexin type 9).
The atherosclerosis prone LDL receptor knockout mice (Ldlr -/-, C57BL/6J background)carry a deletion of the NADP(H)-transhydrogenase gene (Nnt) encoding the mitochondrial enzyme that catalyzes NADPH synthesis.
In this study, we examined the effect of myricetin on lipid accumulation in macrophage and atherosclerosis in atherosclerosis-prone low density lipoprotein receptor-deficient (<i>Ldlr</i><sup>
2, 3, 4', 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms.
Inflammation relevant genes, such as F4/80, tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and monocyte chemoattractant protein (MCP)-1, and lipid metabolism associated gene, such as LDL receptor, class A scavenger receptors (SR-A), scavenger receptor class B type I (SR-BI), CD36, ATP binding cassette subfamily A member 1 (ABCA1), and ATP binding cassette subfamily G member 1 (ABCG1) in the aorta were significantly down-regulated in miR-217 group when compared with atherosclerosis group.
In a large animal model of LDLR deficiency and atherosclerosis, long-term treatment with BemA reduces LDL-C and attenuates the development of aortic and coronary atherosclerosis in both <i>LDLR</i><sup>+/-</sup> and <i>LDLR</i><sup>-/-</sup> miniature pigs.
Here, we used LDL receptor-deficient mice fed a high-fat diet (HFD) for 13 weeks as a model for atherosclerosis and evaluated the effects of continuous administration of HW.
We here examined atherosclerosis development in low-density lipoprotein receptor (LDL-R)-deficient (LDL-R<sup>-/-</sup>) mice with elevated endogenous S1P levels.
Conclusions- This all-in-one AAV-CRISPR vector targeting Ldlr is an effective and versatile tool to model atherosclerosis with a single injection and provides a useful alternative to the use of germline Ldlr-KO mice.
To investigate the impact of these transcriptional changes in atherosclerosis development, we have generated mice carrying a Ser-to-Ala mutation in myeloid cells in the LDL receptor (LDLR)-deficient atherosclerotic background (M-S196A<sup>Ldlr-KO</sup>).