ArticleItalian journal of pediatrics2023
SIGIRR-caspase-8 signaling mediates endothelial apoptosis in Kawasaki disease.
Article in Italian journal of pediatrics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Identification of programmed cell death and mitochondria correlated biomarkers for Kawasaki disease by integrated bioinformatics and machine-learning algorithms with RT-qPCR verification.Frontiers in genetics · 2026Article
- Role of Programmed Cell Death in the Pathogenesis of Kawasaki Disease: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- Toll-like receptors in infectious myocarditis: pathogen-specific recognition, spatiotemporal dynamic regulation and clinical translation.Frontiers in cardiovascular medicine · 2026Review
- The Etiopathogenesis of Kawasaki Disease: Evolving Understanding of Diverse Triggers.Immunity, inflammation and disease · 2025Review
- SIGIRR: An Orphan Receptor Mediating Anti-inflammatory Actions.Expert reviews in molecular medicine · 2025Review
- Impact of intravenous immunoglobulin treatment on peripheral blood cells in children with Kawasaki disease complicated with coronary artery lesion.Italian journal of pediatrics · 2025Article
- Clinical significance of caspase-1 in coronary artery lesions in Kawasaki disease and its mechanism of action on vascular smooth muscle cells.Postepy dermatologii i alergologii · 2025Article
- Cathelicidin (LL-37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling.Immunity, inflammation and disease · 2023Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundKawasaki disease (KD) is a kind of vasculitis with unidentified etiology. Given that the current diagnosis and therapeutic strategy of KD are mainly dependent on clinical experiences, further research to explore its pathological mechanisms is warranted.
methodsEnzyme linked immunosorbent assay (ELISA) was used to measure the serum levels of SIGIRR, TLR4 and caspase-8. Western blotting was applied to determine protein levels, and flow cytometry was utilized to analyze cell apoptosis. Hematoxylin eosin (HE) staining and TUNEL staining were respectively used to observe coronary artery inflammation and DNA fragmentation.
resultsIn this study, we found the level of SIGIRR was downregulated in KD serum and KD serum-treated endothelial cells. However, the level of caspase-8 was increased in serum from KD patients compared with healthy control (HC). Therefore, we hypothesized that SIGIRR-caspase-8 signaling may play an essential role in KD pathophysiology. In vitro experiments demonstrated that endothelial cell apoptosis in the setting of KD was associated with caspase-8 activation, and SIGIRR overexpression alleviated endothelial cell apoptosis via inhibiting caspase-8 activation. These findings were also recapitulated in the Candida albicans cell wall extracts (CAWS)-induced KD mouse model.
conclusionOur data suggest that endothelial cell apoptosis mediated by SIGIRR-caspase-8 signaling plays a crucial role in coronary endothelial damage, providing potential targets to treat KD.
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