ArticleScientific reports2017
Disruption of Endothelial Cell Homeostasis Plays a Key Role in the Early Pathogenesis of Coronary Artery Abnormalities in Kawasaki Disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Losartan Ameliorates Coronary Neointimal Thickening in a Mouse Model of Kawasaki Disease: A Pilot Study.Biomedicines · 2026Article
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Chlorogenic acid alleviates endothelial cell inflammation and apoptosis of Kawasaki disease.European journal of nutrition · 2026Article
- [cGAS-STING signaling pathway in Kawasaki disease: mechanistic insights and advances in clinical applications].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- Identification of Serum BST1 as a Biomarker to Predict Coronary Artery Lesions in Children with Kawasaki Disease Based on 4D-DIA Quantitative Proteomics.Journal of inflammation research · 2026Article
- SESN2 as a Novel Diagnostic and Prognostic Biomarker for Kawasaki Disease and Coronary Artery Lesions.Journal of inflammation research · 2026Article
- LncRNAs in Kawasaki disease and Henoch-Schönlein purpura: mechanisms and clinical applications.Molecular and cellular biochemistry · 2024Review
- Semaphorin 7A promotes endothelial permeability and inflammation via plexin C1 and integrin β1 in Kawasaki disease.BMC pediatrics · 2024Article
- Ferulic acid suppresses the inflammation and apoptosis in Kawasaki disease through activating the AMPK/mTOR/NF-κB pathway.Frontiers in pharmacology · 2024Article
- Protective Roles of Xijiao Dihuang Tang on Coronary Artery Injury in Kawasaki Disease.Cardiovascular drugs and therapy · 2023Article
- The Therapeutic Effects of EFNB2-Fc in a Cell Model of Kawasaki Disease.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Statins Show Anti-Atherosclerotic Effects by Improving Endothelial Cell Function in a Kawasaki Disease-like Vasculitis Mouse Model.International journal of molecular sciences · 2022Article
- Article
- Recent advances in Extracellular Vesicles and their involvements in vasculitis.Free radical biology & medicine · 2021Review
- Kawasaki syndrome: role of superantigens revisited.The FEBS journal · 2021Review
- Overexpressed Neuropilin-1 in Endothelial Cells Promotes Endothelial Permeability through Interaction with ANGPTL4 and VEGF in Kawasaki Disease.Mediators of inflammation · 2021Article
- The role of CaScientific reports · 2020Article
- Neutrophil-Derived Semaphorin 4D Induces Inflammatory Cytokine Production of Endothelial Cells via Different Plexin Receptors in Kawasaki Disease.BioMed research international · 2020Article
- Elevated Levels of Pentraxin 3 Correlate With Neutrophilia and Coronary Artery Dilation During Acute Kawasaki Disease.Frontiers in pediatrics · 2020Article
- Endothelial cell pyroptosis plays an important role in Kawasaki disease via HMGB1/RAGE/cathespin B signaling pathway and NLRP3 inflammasome activation.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of endothelial cell homeostasis may be associated with the pathogenesis of coronary artery abnormalities (CAA) in Kawasaki disease (KD). We sought to clarify the poorly understood pathogenic role of endothelial cell survival and death in KD vasculitis. Human umbilical vein endothelial cells (HUVECs) stimulated with sera from KD patients, compared with sera from patients with bacterial infections, exhibited significant increases in cytotoxicity, high mobility group box protein 1 (HMGB-1), and caspase-3/7 and a decrease in phosphorylated Akt/Akt (pAkt/Akt) ratios. HUVECs stimulated with sera from KD patients treated with immunoglobulin (IG) showed significantly decreased cytotoxicity, HMGB-1, and caspase-3/7 levels and increased pAkt/Akt ratios, as compared with results for untreated HUVECs (P < 0.001, P = 0.008, P = 0.040, and P < 0.001, respectively). In HUVECs stimulated with sera from KD patients, the increased cytotoxicity levels and the suppression of increased pAkt/Akt ratios after subsequent IG treatment were closely related to the development of CAA (P = 0.002 and P = 0.035). Our data reveal that shifting the balance toward cell death rather than survival appears to perturb endothelial cell homeostasis and is closely related to the development of CAA. The cytoprotective effects of IG treatment appear to ameliorate endothelial cell homeostasis.
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