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The TIMP3/Apelin axis Regulates Atherosclerosis and Heart Metabolism leading to increased mortality in ApoE null Mice

ChEBI2015-01-01 更新2026-07-21 收录

动脉粥样硬化机制

心脏代谢研究

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-53548 数据链接链接失效反馈

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The TIMP3/Apelin axis Regulates Atherosclerosis and Heart Metabolism leading to increased mortality in ApoE null Mice

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创建时间：

2015-01-01

动脉粥样硬化机制

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Nicotinic Acid Receptor GPR109A Is Down-Regulated in Human Macrophage-Derived Foam Cells

动脉粥样硬化机制

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Nicotinic acid (NA) regresses atherosclerosis in human imaging studies and reduces atherosclerosis in mice, mediated by myeloid cells, independent of lipoproteins. Since GPR109A is expressed by human

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Gene expression in primary human macrophages and foam cells. Homo sapiens

动脉粥样硬化机制

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The aim of the experiment was to determine the effects of 48 hours of treatment with oxidized low density lipoprotein (oxLDL) on gene expression in primary human monocyte-derived macrophages. Overall

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Table_1_Exploration of Crucial Mediators for Carotid Atherosclerosis Pathogenesis Through Integration of Microbiome, Metabolome, and Transcriptome.DOCX

动脉粥样硬化机制

多组学整合分析

BackgroundCarotid atherosclerosis (CAS) is an important cause of stroke. Although interactions between the gut microbiome and metabolome have been widely investigated with respect to the pathogenesis

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LncRNA ICR regulates endothelium inflammation through feedback activation of NF-κB signaling

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The responsive and abundant lncRNAs to pro-inflammatory factors in human ECs were screened and validated by RNA sequencing and qPCR. ICAM1-related non-coding RNA (ICR) was identified as the most poten

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The TIMP3/Apelin axis Regulates Atherosclerosis and Heart Metabolism leading to increased mortality in ApoE null Mice

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