Single-cell nuclear transcriptome sequencing reveals aspirin inhibits angiogenesis in Kawasaki disease mouse model
10.16438/j.0513-4870.2024-0468
- VernacularTitle:单细胞核转录组测序揭示阿司匹林抑制川崎病小鼠模型心脏组织的血管新生
- Author:
Jing-jing WANG
1
;
Hai-guo YU
2
;
Zhi-dan FAN
2
Author Information
1. Department of Cardiovascular Medicine, Henan Provincial Chest Hospital & Chest Hospital Affiliated to Zhengzhou University, Zhengzhou 450003, China
2. Department of Rheumatology and Immunology, Children′s Hospital of Nanjing Medical University, Nanjing 210008, China
- Publication Type:Research Article
- Keywords:
Kawasaki disease;
coronary artery;
neovascularization;
vascular endothelial growth factor;
macrophage
- From:
Acta Pharmaceutica Sinica
2024;59(10):2809-2819
- CountryChina
- Language:Chinese
-
Abstract:
Kawasaki disease (KD) is an acute systemic vasculitis that primarily affects children. If left untreated in the early stages of the disease, it can lead to coronary artery aneurysms or the formation of arterial fistulae, and in severe cases, myocardial infarction. The pathogenesis of KD is related to the infiltration of immune cells into the walls of the coronary arteries. Macrophages play a crucial role in the development of KD by participating in inflammatory responses and neovascularization. Vascular endothelial growth factor (VEGF) is upregulated in the serum and coronary arteries of patients with KD, promoting inflammation and neovascularization, thereby increasing the risk of aneurysms. Aspirin is one of the standard treatment methods for KD. It exerts anti-inflammatory and anti-thrombotic effects by inhibiting platelet aggregation and reducing inflammatory mediators, thus controlling the acute symptoms of the disease. Animal welfare and experimental procedures follow the regulations of the Animal Ethics Committee of Children′s Hospital of Nanjing Medical University. Single-cell nuclear transcriptome sequencing (snRNA-seq) can provide profound insights into the cellular and molecular landscape of KD. Through snRNA-seq analysis, it was found that aspirin may improve endothelial dysfunction by downregulating VEGF levels in coronary endothelial cells and inhibiting macrophage-mediated proangiogenic signals to endothelial cells, thereby preventing arterial stenosis or aneurysm formation.
