ArticleJournal of inflammation research2021
KCa3.1 Inhibition of Macrophages Suppresses Inflammatory Response Leading to Endothelial Damage in a Cell Model of Kawasaki Disease.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- MicroRNA-125a-5p promotes NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis in endothelial cells during Kawasaki disease.Scientific reports · 2026Article
- Construction and validation of a diagnostic model for Kawasaki disease based on neutrophil-related genes and analysis of immune infiltration.Translational pediatrics · 2026Article
- Targeting STAT3 pathway attenuates macrophages inflammation and cardiovascular injury in a model of Kawasaki disease.Scientific reports · 2026Article
- 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
- Changes in Serum Levels of NINJ1 and HMGB1 in Children with Kawasaki Disease and Their Clinical Significance.Biomedicines · 2026Article
- Genetic silencing of KChannels (Austin, Tex.) · 2025Article
- Neuro-Cancer Interactions Shape Glioma Intratumoral Heterogeneity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Amphiregulin Promotes Proliferation and Migration of the Damaged Endothelial Cells in Kawasaki Disease Cell Models.Immunity, inflammation and disease · 2025Article
- Neonatal Chlamydia muridarum respiratory infection causes neuroinflammation within the brainstem during the early postnatal period.Journal of neuroinflammation · 2024Article
- Regulation of T Lymphocyte Functions through Calcium Signaling Modulation by Nootkatone.International journal of molecular sciences · 2024Article
- M2 macrophage‑derived exosomes alleviate KCa3.1 channel expression in rapidly paced HL‑1 myocytes via the NF‑κB (p65)/STAT3 signaling pathway.Molecular medicine reports · 2024Article
- Challenges in the Therapeutic Targeting of KCa Channels: From Basic Physiology to Clinical Applications.International journal of molecular sciences · 2024Review
- Functional Potassium Channels in Macrophages.The Journal of membrane biology · 2023Review
- The Therapeutic Effects of EFNB2-Fc in a Cell Model of Kawasaki Disease.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Advances in understanding Kawasaki disease-related immuno-inflammatory response and vascular endothelial dysfunction.Pediatric investigation · 2022Review
- Molecular mechanisms of endothelial dysfunction in Kawasaki-disease-associated vasculitis.Frontiers in cardiovascular medicine · 2022Review
- The contribution of ion channels to shaping macrophage behaviour.Frontiers in pharmacology · 2022Review
- Regulatory role of KCa3.1 in immune cell function and its emerging association with rheumatoid arthritis.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMacrophages-mediated inflammation is linked with endothelial damage of Kawasaki disease (KD). KCa3.1, a calcium-activated potassium channel, modulates inflammation of macrophages. However, little is known about the role of KCa3.1 in inflammation by macrophages involved in KD. Hence, this study is aimed to explore the potential role of KCa3.1 in regulating inflammatory response by macrophages and subsequent vascular injury in an in vitro model of KD.
methodsRAW264.7 cells were stimulated with
resultsOur study showed that LCWE increased KCa3.1 protein level in RAW264.7 macrophages and KCa3.1 inhibition by TRAM-34 notably suppressed the expression of pro-inflammatory molecules in LCWE-treated macrophages via blocking the activation of NF-κB and STAT3 pathways. Besides, the inflammation and damage of MCAECs were attenuated in the TRAM-34-treated group compared with the KD model group. This vascular protective role was dependent on the down-regulation of NF-κB and STAT3 signal pathways, which was confirmed by using inhibitors of NF-κB and STAT3.
conclusionThis study demonstrates that KCa3.1 blockade of macrophages suppresses inflammatory reaction leading to mouse coronary artery endothelial cell injury in a cell model of KD by hampering the activation of NF-κB and STAT3 signaling pathway. These findings imply that KCa3.1 may be a potential therapeutic target for 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.