Clinical significance of caspase-1 in coronary artery lesions in Kawasaki disease and its mechanism of action on vascular smooth muscle cells.

INTRODUCTION

Kawasaki disease (KD) is a highly common vascular inflammation in children, with coronary artery lesion (CAL) being one of its most common complications and a key factor for adverse prognosis.

AIM

In this study, we observed the clinical significance of caspase-1 in KD and CAL, and found that caspase-1 was elevated in KD and showed an excellent diagnostic value.

MATERIAL AND METHODS

A prospective analysis was conducted on 67 children with acute KD admitted to our hospital from August 2022 to April 2023 (research group) and 67 healthy outpatient children during the same period (control group). The differences in caspase-1 expression levels between the two study groups were compared, and the diagnostic value of caspase-1 for KD was analyzed using the receiver operating characteristic (ROC) curve. Subsequently, the correlation between caspase-1 and inflammatory factors in the study groups was observed and the diagnostic value of caspase-1 for CAL was analyzed. Subsequently, human coronary artery smooth muscle cells (HCASMCs) were purchased, and caspase-1 aberrant expression vectors were transfected into HCASMCs to detect the proliferation and apoptosis ability of the cells.

RESULTS

Caspase-1 of the research group was higher than that of the control group, and the sensitivity and specificity of caspase-1 for diagnosing the occurrence of KD were 50.75% and 89.55%, respectively ( < 0.05). Pearson correlation coefficients showed a positive correlation between both caspase-1 and inflammatory factors in the research group ( < 0.05). In addition, caspase-1 showed an excellent diagnostic effect on the occurrence of CAL. In assays, elevated caspase-1 expression was seen to promote aberrant proliferation and inhibit apoptosis in HCASMCs ( < 0.05).

CONCLUSIONS

Caspase-1 is elevated in KD and shows an excellent diagnostic value for both KD and the occurrence of CAL in KD patients, possibly through promoting the abnormal proliferation of HCASMCs.