ArticlePediatric cardiology2014
Genetic polymorphism of SMAD5 is associated with Kawasaki disease.
Article in Pediatric cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Etiology Model of Kawasaki Disease and Multisystem Inflammatory Syndromes: Mast Cell Activation.Current issues in molecular biology · 2026Article
- EIF4A3 enhances the viability, invasion and osteogenic differentiation of BMSCs via the USP53/SMAD5 pathway.Scientific reports · 2025Article
- Involvement of USP7 in aggravating Kawasaki disease by promoting TGFβ2 signaling mediated endothelial-mesenchymal transition and coronary artery remodeling.International immunopharmacology · 2025Article
- Genetic Polymorphisms in the 3'-Untranslated Regions ofBiomedicines · 2022Article
- Predictive model based on gene and laboratory data for intravenous immunoglobulin resistance in Kawasaki disease in a Chinese population.Pediatric rheumatology online journal · 2021Article
- Immunogenetics of Kawasaki disease.Clinical reviews in allergy & immunology · 2020Review
- Long noncoding RNA SMAD5-AS1 acts as a microRNA-106a-5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Dissecting Kawasaki disease: a state-of-the-art review.European journal of pediatrics · 2017Review
- Association of PECAM-1 Gene Polymorphisms with Kawasaki Disease in Chinese Children.Disease markers · 2017Article
- Update of genetic susceptibility in patients with Kawasaki disease.Korean journal of pediatrics · 2015Review
- Interleukin 10 and Transforming Growth Factor Beta Polymorphisms as Risk Factors for Kawasaki Disease: A Case-Control Study and Meta-Analysis.Avicenna journal of medical biotechnologyArticle
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mothers against decapentaplegic homolog (SMAD) proteins are intracellular mediators of members of the transforming growth factor-β (TGF-β) superfamily, which are activated by bone morphogenetic proteins (BMPs). On activation, SMAD5 forms heterometric SMAD complexes, which are translated to the nucleus where they regulate gene transcription. TGF-β induces T cell activation and cardiovascular disease, two important features of Kawasaki disease (KD), whereas BMP is associated with coronary artery disease. In this study, we hypothesized that single nucleotide polymorphisms (SNPs) of SMAD5 may be associated with KD and coronary arterial lesions (CALs). Genotyping for 15 SNPs of the SMAD5 gene (rs3764941, rs10085013, rs6596284, rs7356756, rs13179769, rs13166063, rs1109158, rs4585442, rs4146185, rs12719481, rs6865297, rs3206634, rs6871224, rs1057898, and rs7031) was performed by direct sequencing of 105 KD patients and 303 healthy adult controls. We also compared the allele frequencies between a CAL group (n = 31) and a normal coronary group (n = 74). Results showed that among the 15 SNPs, rs3206634 was significantly associated with KD in a recessive model (odds ratio = 2.31, p = 0.019), whereas there was no association between any of the 15 SNPs and CALs. These findings may be used as a risk factors development of KD or for future generations of therapeutic treatments for KD.
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