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KLF4 Dependent Phenotypic Modulation of SMCs Plays a Key Role in Regulating Plaque Pathogenesis

ChEBI2015-04-24 更新2026-07-21 收录

动脉粥样硬化机制

平滑肌细胞表型调控

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-65812 数据链接链接失效反馈

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KLF4 Dependent Phenotypic Modulation of SMCs Plays a Key Role in Regulating Plaque Pathogenesis

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创建时间：

2015-04-24

动脉粥样硬化机制

单细胞RNA测序

Raw fastq files from paired-end, Illumina-based sequencing on NovaSeq6000 Apoe-/- mice were fed a western diet for 4 weeks and administered saline or nt-LNA (30 mg/kg) weekly. After 4 weeks, aortic a

NIAID Data Ecosystem80

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

动脉粥样硬化机制

泡沫细胞

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

NIAID Data Ecosystem40

Down-regulation of single-stranded DNA-binding protein 1 expression induced by HCMV infection promotes lipid accumulation in cells

脂代谢与病毒感染

动脉粥样硬化机制

The objective of this study was to observe the infection of human cytomegalovirus (HCMV) to human umbilical vein endothelial cells, and its effect on the expression of single-stranded DNA-binding prot

NIAID Data Ecosystem30

Activation of the pluripotency factor OCT4 in smooth muscle cells is atheroprotective. doi: 10.1038/nm.4109

动脉粥样硬化机制

平滑肌细胞转录组

The multiple claims about reactivation of the embryonic stem cell (ESC) pluripotency factor OCT4 in somatic cells are highly controversial due to the fact that there is no direct evidence that OCT4 ha

NIAID Data Ecosystem70

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

动脉粥样硬化机制

血管炎症调控

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

NIAID Data Ecosystem40

KLF4 Dependent Phenotypic Modulation of SMCs Plays a Key Role in Regulating Plaque Pathogenesis

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