ArticleCirculation research2020
Reduced Platelet miR-223 Induction in Kawasaki Disease Leads to Severe Coronary Artery Pathology Through a miR-223/PDGFRβ Vascular Smooth Muscle Cell Axis.
Article in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 3 of them syntheses that pooled it.
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Who cites it
50 citing papers in PubMed, 3 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Comparative efficacy of platelet-rich plasma monotherapy versus combination therapies for knee osteoarthritis: a systematic review and network meta-analysis.Journal of orthopaedic surgery and research · 2026Pooled it
- The role of microRNAs in Kawasaki disease: a systematic review.European journal of pediatrics · 2026Pooled it
- MicroRNAs in Kawasaki disease: An update on diagnosis, therapy and monitoring.Frontiers in immunology · 2022Pooled it
- Protective Effects of Jiawei Baihu Tang in Kawasaki Disease: Omics Analysis and Mechanistic Exploration.Cardiovascular drugs and therapy · 2026Article
- Clinical role and mechanism of miR-4443 in coronary heart disease: a prognostic marker and regulator of vascular smooth muscle cell Function.Journal of cardiothoracic surgery · 2026Article
- Review
- T-cadherin deprivation in endothelial cells promotes vascular injury in Kawasaki disease through SOD2/ROS/NLRP3 pathway-mediated pyroptosis.Journal of molecular cell biology · 2026Article
- Review
- Impact of breastfeeding andFrontiers in immunology · 2026Article
- Effectiveness of Initial Corticosteroid Treatment in Kawasaki Disease Children Suspected to be IVIG Resistant.Pediatric cardiology · 2025Observational
- Platelet-Monocyte Aggregate Instigates Inflammation and Vasculopathy in Kawasaki Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Age-Specific Cardiovascular and Platelet Dynamics in Kawasaki Disease.International journal of general medicine · 2025Article
- Lysophosphatidylcholine as a Novel Diagnostic Biomarker in Kawasaki Disease: Based on Immunometabolism-Related Signature.Journal of inflammation research · 2025Article
- Combination of CRP and miRNA signature as a potential diagnostic strategy for Kawasaki disease.Frontiers in pediatrics · 2025Article
- The Central Role of Interleukin-1 Signalling in the Pathogenesis of Kawasaki Disease Vasculitis: Path to Translation.The Canadian journal of cardiology · 2024Review
- mTOR signalling controls the formation of smooth muscle cell-derived luminal myofibroblasts during vasculitis.EMBO reports · 2024Article
- Statin suppresses the development of excessive intimal proliferation in a Kawasaki disease mouse model.Physiological reports · 2024Article
- Platelets in Kawasaki disease: mediators of vascular inflammation.Nature reviews. Rheumatology · 2024Review
- Differential expression of miR-140-3p and its potential role during the development of the acute coronary syndrome.Irish journal of medical science · 2024Article
- Targeting deubiquitinase OTUB1 protects vascular smooth muscle cells in atherosclerosis by modulating PDGFRβ.Frontiers of medicine · 2024Article
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Authors and funding
16 authors at 2 institutions in 3 countries.
Funding
Abstract
rationaleKawasaki disease (KD) is an acute vasculitis of early childhood that can result in permanent coronary artery structural damage. The cause for this arterial vulnerability in up to 15% of patients with KD is unknown. Vascular smooth muscle cell dedifferentiation play a key role in the pathophysiology of medial damage and aneurysm formation, recognized arterial pathology in KD. Platelet hyperreactivity is also a hallmark of KD. We recently demonstrated that uptake of platelets and platelet-derived miRNAs influences vascular smooth muscle cell phenotype in vivo.
objectiveWe set out to explore whether platelet/vascular smooth muscle cell (VSMC) interactions contribute to coronary pathology in KD. METHODS AND
resultsWe prospectively recruited and studied 242 patients with KD, 75 of whom had documented coronary artery pathology. Genome-wide miRNA sequencing and droplet digital PCR demonstrated that patient with KD platelets have significant induction of miR-223 compared with healthy controls (HCs). Platelet-derived miR-223 has recently been shown to promote vascular smooth muscle quiescence and resolution of wound healing after vessel injury. Paradoxically, patients with KD with the most severe coronary pathology (giant coronary artery aneurysms) exhibited a lack of miR-223 induction. Hyperactive platelets isolated from patients with KD are readily taken up by VSMCs, delivering functional miR-223 into the VSMCs promoting VSMC differentiation via downregulation of PDGFRβ (platelet-derived growth factor receptor β). The lack of miR-223 induction in patients with severe coronary pathology leads to persistent VSMC dedifferentiation. In a mouse model of KD (
conclusionsPlatelet-derived miR-223 (through PDGFRβ inhibition) promotes VSMC differentiation and resolution of KD induced vascular injury. Lack of miR-223 induction leads to severe coronary pathology characterized by VSMC dedifferentiation and medial damage. Detection of platelet-derived miR-223 in patients with KD (at the time of diagnosis) may identify patients at greatest risk of coronary artery pathology. Moreover, targeting platelet miR-223 or VSMC PDGFRβ represents potential therapeutic strategies to alleviate coronary pathology in KD. Graphic Abstract: A graphic abstract is available for this article.
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