ArticleBioMed research international2022
Regulation of Atherosclerosis by Toll-Like Receptor 4 Induced by Serum Amyloid 1: A Systematic In Vitro Study.
Article in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- SASP-driven vascular aging: unraveling the transcriptional nexus in endothelial senescence and cardiovascular disease.Histochemistry and cell biology · 2026Review
- Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026Review
- High‑fat diet‑induced LCN2 exacerbates myocardial ischemia‑reperfusion injury by enhancing platelet activation.Molecular medicine reports · 2024Article
- ApoM binds endotoxin contributing to neutralization and clearance by High Density Lipoprotein.Biochemistry and biophysics reports · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to investigate the effects of serum amyloid 1 (SAA1) on activation of endothelial cells, formation of foam cells, platelet aggregation, and monocyte/platelet adhesion to endothelial cells. The effect of SAA1 on the inflammatory activation of endothelial cells was investigated by detecting the expression of inflammatory factors and adhesion molecules. The role of SAA1 in formation of foam cells was verified by detecting lipid deposition and expression of molecules related to the formation of foam cells. After platelets were stimulated by SAA1, the aggregation rate was evaluated to determine the effect of SAA1 on platelet aggregation. Monocytes/platelets were cocultured with human umbilical vein endothelial cells (HUVECs) pretreated with or without SAA1 to determine whether SAA1 affected monocyte/platelet adhesion to endothelial cells. By inhibiting toll-like receptor 4 (TLR4) function, we further identified the role of TLR4 signaling in SAA1-mediated endothelial inflammatory activation, foam-cell formation, and monocyte/platelet adhesion to HUVECs. SAA1 significantly increased the expression of adhesion molecules and inflammatory factors in HUVECs. Moreover, SAA1 also promoted lipid deposition and the expression of inflammatory factors and low-density lipoprotein receptor-1 (LOX-1) in THP-1-derived macrophages. In addition, SAA1 induced platelet aggregation and enhanced monocyte/platelet adhesion to HUVECs. However, the TLR4 antagonist significantly inhibited SAA1-induced endothelial cell activation, foam-cell formation, and monocyte/platelet adhesion to HUVECs and downregulated the expression of myeloid differentiation factor 88 (MyD88), phosphor-inhibitor of nuclear factor
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Registered trials
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