# Changes in Serum Levels of NINJ1 and HMGB1 in Children with Kawasaki Disease and Their Clinical Significance

**Authors:** Tong Tong, Ting Zhao, Jiawen Xu, Fei Liu, Linghao Cai, Xinrui Mao, Chunhong Xie, Yujia Wang, Fangqi Gong

PMC · DOI: 10.3390/biomedicines14020402 · Biomedicines · 2026-02-10

## TL;DR

This study finds that elevated levels of NINJ1 and HMGB1 in children with Kawasaki disease are linked to coronary artery lesions and may help diagnose the condition.

## Contribution

The study identifies NINJ1 and HMGB1 as potential biomarkers for Kawasaki disease and its complications.

## Key findings

- Serum NINJ1 and HMGB1 levels were significantly higher in Kawasaki disease patients compared to controls.
- NINJ1 levels correlated with coronary artery z-scores and were elevated in patients with coronary artery lesions.
- NINJ1 and HMGB1 levels showed a strong positive correlation in Kawasaki disease patients.

## Abstract

Purpose: Kawasaki disease (KD) is an acute systemic vasculitis that can result in coronary artery lesions (CALs). This study aims to explore the expression levels of serum Ninjurin-1 (NINJ1) and high-mobility group box 1 (HMGB1) in the acute phase of KD and evaluate their clinical significance. Methods: A total of 180 children were enrolled, comprising 113 KD patients, 35 healthy controls (HCs), and 32 febrile controls whose clinical data were collected. Serum levels of NINJ1, HMGB1, Lactate Dehydrogenase (LDH), and routine inflammatory markers were compared across groups. Serum levels of NINJ1 and HMGB1 were measured via ELISA. Correlations were analyzed using Spearman tests. The diagnostic and predictive performance of biomarkers was assessed using Receiver Operating Characteristic (ROC) curve analyses. Results: Serum levels of NINJ1 and HMGB1 were significantly elevated in the KD group compared with both the HC and FC groups (all p < 0.001). NINJ1 levels were positively correlated with the z-scores of coronary arteries and were significantly higher in the CAL subgroup than in the non-CAL subgroup (p = 0.004). A strong positive correlation was observed between serum NINJ1 and HMGB1 levels in the KD group (p < 0.001). Conclusions: Elevated serum NINJ1 levels during the acute phase of KD were associated with the presence of CALs, while HMGB1 shows promise in differentiating KD from other febrile illnesses. These findings collectively suggest that the NINJ1-HMGB1 axis may offer novel insights into the mechanisms underlying KD vasculitis, supporting further investigation into its potential clinical relevance.

## Linked entities

- **Genes:** NINJ1 (ninjurin 1) [NCBI Gene 4814], HMGB1 (high mobility group box 1) [NCBI Gene 3146]
- **Diseases:** Kawasaki disease (MONDO:0012727)

## Full-text entities

- **Genes:** HMGB1 (high mobility group box 1) [NCBI Gene 3146] {aka HMG-1, HMG1, HMG3, SBP-1}, IFNA1 (interferon alpha 1) [NCBI Gene 3439] {aka IFL, IFN, IFN-ALPHA, IFN-alphaD, IFNA13, IFNA@}, IFNA17 (interferon alpha 17) [NCBI Gene 3451] {aka IFN-alphaI, IFNA, INFA, LEIF2C1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NINJ1 (ninjurin 1) [NCBI Gene 4814] {aka NIN1, NINJURIN, hNINJ1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, CA8 (carbonic anhydrase 8 (inactive)) [NCBI Gene 767] {aka CA-RP, CA-VIII, CALS, CAMRQ3, CARP, SCAR34}, CALCA (calcitonin related polypeptide alpha) [NCBI Gene 796] {aka CALC1, CGRP, CGRP-I, CGRP-alpha, CGRP1, CT}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** heart disease (MESH:D006331), systemic vasculitis (MESH:D056647), systemic (MESH:D015619), coronary artery damage (MESH:D003324), FC (MESH:C536209), KD (MESH:D009080), thrombocytosis (MESH:D013922), sepsis (MESH:D018805), necrosis (MESH:D009336), coronary artery aneurysms (MESH:D003323), thrombotic (MESH:D013927), AAA (MESH:D017544), urinary tract infection (MESH:D014552), rheumatic or other immune system diseases (MESH:D007154), thrombocytopenia (MESH:D013921), cardiovascular disease (MESH:D002318), dilation (MESH:D002311), sudden death (MESH:D003645), hypoalbuminemia (MESH:D034141), febrile (MESH:D000071072), vessel wall lesions (MESH:D065708), bronchopneumonia or pneumonia (MESH:D001996), systemic lupus erythematosus (MESH:D008180), febrile illnesses (MESH:D005334), coronary endothelial dysfunction (MESH:D003327), HC (MESH:D000067329), Inflammatory (MESH:D007249), conditions (MESH:D020763), vasculitis (MESH:D014657), injury (MESH:D014947), lupus nephritis (MESH:D008181), endothelial dysfunction (MESH:D014652), aneurysm (MESH:D000783)
- **Chemicals:** NA (MESH:D012964), RX105287H (-)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12938374/full.md

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12938374/full.md

## References

24 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938374/full.md

---
Source: https://tomesphere.com/paper/PMC12938374