ArticleJournal of the American Heart Association2017
Bone Marrow-Derived MicroRNA-223 Works as an Endocrine Genetic Signal in Vascular Endothelial Cells and Participates in Vascular Injury From Kawasaki Disease.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- MicroRNAs in Kawasaki disease: An update on diagnosis, therapy and monitoring.Frontiers in immunology · 2022Pooled it
- Role of Programmed Cell Death in the Pathogenesis of Kawasaki Disease: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- Exploring the role of exosomal and non-exosomal non-coding RNAs in Kawasaki disease: Implications for diagnosis and therapeutic strategies against coronary artery aneurysms.Biochemistry and biophysics reports · 2025Review
- The Central Role of Interleukin-1 Signalling in the Pathogenesis of Kawasaki Disease Vasculitis: Path to Translation.The Canadian journal of cardiology · 2024Review
- Circulating and Cardiac Tissue miRNAs in Children with Dilated Cardiomyopathy.Journal of cardiovascular development and disease · 2023Article
- Diagnosis, Progress, and Treatment Update of Kawasaki Disease.International journal of molecular sciences · 2023Review
- MiR-223-3p affects the proliferation and apoptosis of HCAECs in Kawasaki disease by regulating the expression of FOXP3.Immunity, inflammation and disease · 2023Article
- CircRNA7632 down-regulation alleviates endothelial cell dysfunction in Kawasaki disease via regulating IL-33 expression.Cell stress & chaperones · 2023Article
- Oxidative Stress and Epigenetics: miRNA Involvement in Rare Autoimmune Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- SIGIRR-caspase-8 signaling mediates endothelial apoptosis in Kawasaki disease.Italian journal of pediatrics · 2023Article
- Identifying differentially expressed genes and miRNAs in Kawasaki disease by bioinformatics analysis.Scientific reports · 2022Article
- Circulating microRNAs in patients with aneurysmal dilatation of coronary arteries.Experimental and therapeutic medicine · 2022Article
- Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease.Frontiers in immunology · 2022Article
- Molecular mechanisms of endothelial dysfunction in Kawasaki-disease-associated vasculitis.Frontiers in cardiovascular medicine · 2022Review
- The rs7404339 AA Genotype inFrontiers in cardiovascular medicine · 2022Article
- MicroRNA-197-3p mediates damage to human coronary artery endothelial cells via targeting TIMP3 in Kawasaki disease.Molecular and cellular biochemistry · 2021Article
- IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway.Cell death & disease · 2021Article
- Epigenetics in Kawasaki Disease.Frontiers in pediatrics · 2021Review
- Article
- miR-223: An Effective Regulator of Immune Cell Differentiation and Inflammation.International journal of biological sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundKawasaki disease (KD) is now the most common cause of acquired cardiac disease in children due to permanent coronary artery damage with unknown etiology. The study sought to determine the role of blood microRNA miR-223 in KD and KD-induced injuries in vascular endothelial cells (ECs) as well as the mechanisms involved. METHODS AND
resultsMicroRNA profiles in serum from patients with KD and from healthy controls were assessed by microarray analysis. We noted that multiple serum microRNAs were aberrantly expressed in KD, among them miR-223, which was the most upregulated abundant serum microRNA. We found that bone marrow-derived blood cells (leukocytes and platelets) were able to secrete miR-223 into serum. Vascular ECs had no endogenous miR-223; however, the blood cell-secreted serum miR-223 could enter into the vascular ECs in the vascular walls. The exogenous miR-223 had strong biological effects on EC functions via its target genes such as IGF1R. Interestingly, KD-induced EC injuries were related to increased miR-223 because they were inhibited by miR-223 knockdown. Finally, these observations were verified using miR-223 knockout mice and the chimeric mice generated by transplantation of bone marrow from miR-223 knockout mice into wild-type mice.
conclusionsIn KD patients, the levels of blood cell-derived miR-223 in ECs are significantly increased. The increased miR-223 in ECs could work as a novel endocrine genetic signal and participate in vascular injury of KD. MiR-223 may provide a novel mechanism and a new therapeutic target for vascular complication of KD.
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