ArticleOpen life sciences2023
PTX3 promotes IVIG resistance-induced endothelial injury in Kawasaki disease by regulating the NF-κB pathway.
Article in Open life sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- [Gut-vascular axis in Kawasaki disease: short-chain fatty acid-mediated immune regulation and therapeutic targets].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- Exosome-Mediated Macrophage Polarization in Gastric Cancer: Inflammatory and Neuroinflammatory Mechanisms and Therapeutic Potential.International journal of general medicine · 2026Review
- Research on gamma globulin unresponsive Kawasaki disease: A review.World journal of clinical pediatrics · 2025Review
- Single-cell transcriptomic analysis reveals a systemic immune dysregulation in intravenous immunoglobulin non-responsive Kawasaki disease.Frontiers in immunology · 2025Article
- Prognostic Value of Pentraxin3 Protein Expression in Human Malignancies: A Systematic Review and Meta-Analysis.Cancers · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intravenous immunoglobulin (IVIG) resistance leads to serious complications in Kawasaki disease (KD) with no effective treatment. This study aimed to investigate the effects of pentraxin 3 (PTX3) on human coronary artery endothelial cells (HCAECs). PTX3 levels were measured using quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assay, and western blotting. Cell viability was detected using the MTT assay. Biological functions were analyzed using CCK-8, EdU, flow cytometry, TUNEL, and qRT-PCR. The levels of factors of the NF-κB pathway were examined using western blotting. The results demonstrated that PTX3 expression was highest in patients and HCAECs with IVIG-resistance. Knockdown of PTX3 promoted proliferation and suppressed apoptosis and inflammation of IVIG-resistant HCAECs, whereas PTX3 overexpression produced the opposite results. Moreover, PTX3 activated the NF-κB pathway in IVIG-resistant HCAECs. A rescue study showed that PTX3 modulated biological behaviors by regulating the NF-κB pathway. Overall, our findings demonstrate that PTX3 promotes IVIG resistance-induced endothelial injury by activating the NF-κB pathway, suggesting that PTX3 may become a novel therapeutic target for patients with IVIG-resistant KD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.