Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IL-1β inhibition partially negates the beneficial effects of diet-induced lipid lowering

ABSTRACT: Thromboembolic events secondary to rupture or erosion of advanced atherosclerotic lesions are the leading cause of death in the world. The most common and effective means to reduce these major adverse cardiovascular events (MACE), including myocardial infarction (MI) and stroke, is aggressive lipid lowering via a combination of drugs and dietary modifications. However, little is known regarding the effects of reducing dietary lipids on the composition and stability of advanced atherosclerotic lesions, the mechanisms that regulate these processes, and what therapeutic approaches might augment the benefits of lipid lowering.

ORGANISM(S): Mus musculus

PROVIDER: GSE264253 | GEO | 2024/05/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cholesterol lowering depletes smooth muscle cell-derived fibromyocytes and chondromyocytes from atherosclerotic lesions

Project description:Study of the effect of low-density lipoprotein (LDL)-lowering therapies on the heterogeneous population of proliferating smooth muscle cells (SMCs) derived from atherosclerotic plaques in an atherosclerotic mouse model by inducing hypercholesterolemia followed by high or low fat diet.

2023-12-08 | E-MTAB-12019 | biostudies-arrayexpress

Cholesterol lowering depletes smooth muscle cell-derived fibromyocytes and chondromyocytes from atherosclerotic lesions

Project description:Cholesterol lowering depletes smooth muscle cell-derived fibromyocytes and chondromyocytes from atherosclerotic lesions

| PRJEB55086 | ENA

Decoding the immune checkpoint signatures in human atherosclerosis: implications of type 2 diabetes and lipid-lowering intervention [human_PBMC_CITEseq]

Project description:Immune checkpoint inhibitor (ICI) therapies in cancer accelerate atherosclerosis progression. Here, we have charted the landscape of immune checkpoint gene expression and defined the network of disease-relevant interactions with single-cell resolution. We found that signaling through PD-1 and CTLA4 is driven by a population of dendritic cells enriched for FSCN1 that can be derived from peripheral blood cells following anti-PD-1 or -CTLA4 treatment ex vivo. Type 2 diabetes dampened plaque PD-1 and CTLA4 signaling, showing that cardiometabolic comorbidities elicit unique responses to ICIs. Lipid-lowering therapy equalized the intensity and direction of immune checkpoint interactions in human blood, while atherosclerotic mice subjected to a lipid-lowering diet displayed both increased co-inhibitory signaling and a downregulation of inflammatory transcriptional programs in plaques. Our findings underscore the potential of lipid-lowering therapies in stabilizing immune checkpoint interactions and reducing plaque inflammation, offering new insights on atherosclerosis and cardiovascular risks in cancer patients undergoing ICI treatments.

2024-12-18 | GSE246317 | GEO

Decoding the immune checkpoint signatures in human atherosclerosis: implications of type 2 diabetes and lipid-lowering intervention [human_carotid_plaque]

2024-12-18 | GSE246315 | GEO

Decoding the immune checkpoint signatures in human atherosclerosis: implications of type 2 diabetes and lipid-lowering intervention [mouse_plaque_scRNAseq]

2024-10-07 | GSE246316 | GEO

Decoding the immune checkpoint signatures in human atherosclerosis: implications of type 2 diabetes and lipid-lowering intervention [human PBMC scRNA-Seq]

2024-12-18 | GSE272294 | GEO

Adenosine-rich extract of Ganoderma lucidum: a safe and effective lipid-lowering substance via regulating expression and modulation of PPAR signaling pathway

Project description:Ganoderma lucidum is a traditional Chinese medicine with a variety of active compounds and possessing adequate lipid-lowering and anti-atherosclerotic effects. However, its main active components and potential mechanisms still remain unclear. Here, we evaluated the anti-hyperlipidemic effect of the adenosine extract from Ganoderma lucidum (AEGL) in high-fat-diet (HFD)-induced hyperlipidemic ApoE-/- mice and explored the underlying biological mechanism by multi-omics analysis. Treatment with AEGL for 8 weeks significantly decreased the serum levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-c) by 45.59%, 41.22%, and 39.02%, respectively, as well as reduced liver TC and TG by 44.15% and 76.23%, compared with the HFD-only group. We also observed significant amelioration of hepatic steatosis without liver and kidney damage after AEGL treatment. Regulating the expression and acetylation/crotonylation of proteins involved in the PPAR signaling pathway may be one of the potential mechanisms involved in the observed lipid-lowering effects of AEGL.

2023-03-11 | PXD036478 | Pride

LncRNA expression in the formation of carotid plaque caused by atherosclerosis

Project description:Atherosclerotic plaques belong to the common vascular disease in the aged, which rupture will lead to acute thromboembolic diseases, the major reason for fatal cardiovascular events. Accumulating evidence indicates that lncRNAs exert critical functions in atherosclerosis. To identify novel astherosclerotic plaques-relevant lncRNAs, four specimens of carotid atherosclerotic plaque were collected, and endovascular tissue one centimeter far from the carotid atherosclerotic plaque was taken as a control group, we performed lncRNA microarray analysis using Affymetrix Human OElncRNA

2022-07-01 | GSE207252 | GEO

siRNAs induced long-term liver ApoB mRNA knockdown significantly lowers serum cholesterol in a mouse model with human-like serum lipids

Project description:Increased serum apoB and associated low density lipoprotein cholesterol (LDL) levels are well correlated with an increased risk of coronary disease. Apo E-/- and LDLr -/- mice have been extensively used for studies of coronary atherosclerosis. These animals show atherosclerotic lesions similar to those in humans, but their serum lipids are low in apoB containing LDL particles. We describe the development of a new mouse model with a human-like lipid profile. Ldlr+/- CETP+/- hemizygous mice carry a single copy of the human CETP transgene and a single copy of a LDL receptor mutation. To evaluate the apoB pathways in this mouse model, we used novel siRNAs formulated in lipid nanoparticles (LNPs). ApoB siRNAs induced up to 95% reduction of liver ApoB mRNA and serum apoB protein, and a significant lowering of serum LDL in Ldlr+/- CETP+/- mice. ApoB targeting is specific, dose dependent and shows lipid lowering effects for over three weeks. Although specific TGs were affected by ApoB KD, and the total plasma lipid levels were decreased by 70%, the overall lipid distribution did not change. Results presented here demonstrate a new mouse model for investigating additional targets within the ApoB pathways using the siRNA modality. Two oligoes specific for ApoB were used to knock down apoB expression in C57Bl6 or B6-Ldlr(tm1)Tg(APOA1-CETP) mice. Gene expression profiling was performed with Affymetrix Merck Custom Mouse 1.0 microarrays (GPL9734).

2010-11-22 | E-GEOD-23088 | biostudies-arrayexpress

GOLDN: Genetics of Lipid Lowering Drugs and Diet Network Study

Project description:GOLDN: Genetics of Lipid Lowering Drugs and Diet Network Study

| PRJNA546418 | ENA