ArticleTranslational pediatrics2022
Kawasaki disease: lncRNA Slco4a1 regulates the progression of human umbilical vein endothelial cells by targeting the miR-335-5p/POU5F1 axis.
Article in Translational pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.
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Who cites it
6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 10 citations in OpenAlex.
- The role of microRNAs in Kawasaki disease: a systematic review.European journal of pediatrics · 2026Pooled it
- Role of long non-coding RNAs and circular RNAs in kawasaki disease: a systematic review.Pediatric rheumatology online journal · 2025Pooled it
- Single-cell transcriptomics uncovers endothelial progenitor-like remodelling driving human coronary atherosclerosis progression.Nature cell biology · 2026Article
- 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
- LncRNAs in Kawasaki disease and Henoch-Schönlein purpura: mechanisms and clinical applications.Molecular and cellular biochemistry · 2024Review
- CircRNA7632 down-regulation alleviates endothelial cell dysfunction in Kawasaki disease via regulating IL-33 expression.Cell stress & chaperones · 2023Article
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
Background: Kawasaki disease (KD) is an autoimmune disease with systemic vasculitis as the main pathological change, and is most common in children under 5. The role of long non-coding RNAs (lncRNAs) in human diseases has been highlighted. LncRNA Slco4a1 was reported to promote cell growth and act as an oncogenic regulator in cancer. However, the role of lncRNA Slco4a1 in KD remains unclear. This study aimed to investigate the role and mechanism of lncRNA Slco4a1 in KD. Methods: Enzyme linked immunosorbent assay (ELISA), qRT-PCR, Western blot, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining were conducted to explore the function of lncRNA Slco4a1. The interaction between POU5F1 and miR-335-5p was analyzed by the RIP assay and dual luciferase assay. Results: LncRNA Slco4a1 was significantly upregulated in the serum of KD patients compared with healthy controls. LncRNA Slco4a1 was upregulated in human umbilical vein endothelial cells (HUVECs) stimulated with KD serum. LncRNA Slco4a1 overexpression could promote the expression of inflammatory factors and apoptosis in HUVECs. The number of inflammatory cells and the infiltration area of the coronary artery in KD rats were decreased after lncRNA Slco4a1 silencing. Furthermore, lncRNA Slco4a1 is a sponge of miR-335-5p and negatively regulated the expression of miR-335-5p. POU5F1 was the downstream target of miR-335-5p, and miR-335-5p overexpression could upregulate the expression of POU5F1. Additionally, miR-335-5p overexpression could inhibit the expression of inflammatory factors and apoptosis in HUVECs. We further investigated the effect of lncRNA Slco4a1 on the mitogen-activated protein kinase (MAPK) signaling pathway, and the results showed that lncRNA Slco4a1 could promote the activation of the MAPK signaling pathway. Conclusions: Together, these results indicated that lncRNA Slco4a1 could regulate the progression of HUVECs in KD by targeting the miR-335-5p/POU5F1 axis, providing new insights for KD treatment.
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