ArticleImmunity, inflammation and disease2026
NLRP3 Inflammasome Activation Mediates Coronary Artery Lesions in Kawasaki Disease by Inducing Endothelial Cells Pyroptosis and Glycocalyx Injury.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- NLRP3 Inflammasome Activation Mediates Coronary Artery Lesions in Kawasaki Disease by Inducing Endothelial Cells Pyroptosis and Glycocalyx Injury.Immunity, inflammation and disease · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
introductionTo investigate the mechanism by which NOD-like receptor heat protein domain-associated protein 3 (NLRP3) activation mediates coronary endothelial dysfunction at different stages of Kawasaki disease (KD).
methodsBlood samples were collected from patients in the acute stage and convalescent stage of KD, as well as healthy/febrile controls. The mRNA expression of NLRP3 and Caspase-1 were detected by qRT-PCR. Serum levels of IL-1β, syndecan-1 (SDC-1), hyaluronic acid (HA), metalloproteinase-9 (MMP-9), and metalloproteinase-1 (TIMP-1) were quantified via ELISA, and Spearman correlation analysis was conducted. In vitro, human coronary artery endothelial cells (HCAECs) were treated with KD patient serum combined with NLRP3 activator/inhibitor treatment. Cell viability (CCK-8) and cell migration (Transwell) were assessed. The relative protein expression of pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD-N) were detected by Western blot. The concentrations of cytokine secretion (IL-1β/IL-18), matrix metabolism (MMP-9/TIMP-1), glycocalyx components (SDC-1/HA) were evaluated by ELISA.
resultsThe levels of NLRP3 mRNA, Caspase-1 mRNA, IL-1β, MMP-9, TIMP-1, SDC-1 and HA in patients with acute KD were significantly higher than those in the healthy/febrile control group (p < 0.01), and these indicators were positively correlated with NLRP3 activation (p < 0.01). KD serum significantly suppressed the proliferation/migration of HCAEC (p < 0.01), induced pyroptosis (upregulated NLRP3/Caspase-1/GSDMD-N), and increased IL-1β/IL-18 secretion with concomitant elevated levels of MMP-9/TIMP-1/SDC-1/HA. NLRP3 inhibitors can reverse the above-mentioned damaging effects (p < 0.01).
conclusionsNLRP3 inflammasome activation during the progression of KD can cause coronary endothelial injury by inducing inflammatory imbalance, endothelial cells pyroptosis, and glycocalyx injury. Targeting NLRP3 represents a promising therapeutic strategy.
Indexed as
Identifiers
What OpenQuestion holds
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.