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Research progress on molecular mechanisms of coronary artery lesions in Kawasaki disease

Published on May. 28, 2025Total Views: 124 times Total Downloads: 24 times Download Mobile

Author: MA Yaxin 1 ZHU Xiaowei 1 LI Shuqiong 1 LI Yunxiang 1 SUN Yonghong 2

Affiliation: 1. First School of Clinical Medical, Gansu University of Chinese Medicine, Lanzhou 730000, China 2. Department of Pediatrics, Gansu Provincial Hospital, Lanzhou 730000, China

Keywords: Kawasaki disease Coronary artery lesions NF-κB S100A12 CaN/NFAT

DOI: 10.12173/j.issn.1004-4337.202501015

Reference: Ma YX, Zhu XW, Li SQ, Li YX, Sun YH. Research progress on molecular mechanisms of coronary artery lesions in Kawasaki disease[J]. Journal of Mathematical Medicine, 2025, 38(5): 390-396. DOI: 10.12173/j.issn.1004-4337.202501015[Article in Chinese]

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Abstract

Kawasaki disease is the most common cardiovascular disease in children, characterized mainly by systemic vasculitis, with coronary artery lesions (CAL) as its major complication, significantly increases the risk of long-term cardiovascular events. The pathogenesis of CAL is complex, involving several signaling pathways such as inflammatory response, immune regulation and endothelial injury, but its underlying mechanism has not been fully elucidated. In recent years, researches about the role of nuclear factor kappa-B (NF-κB), S100 calc-binding protein A12 (S100A12), calcineurin (CaN)/nuclear factors of activated T cells (NFAT) signaling pathway in Kawasaki disease have made some progress, providing important clues for revealing the pathogenesis of CAL in Kawasaki disease. This paper reviewed the research progress of the above signaling pathways, aiming to deepen the understanding of the molecular mechanism of CAL in Kawasaki disease and provide reference for future clinical intervention.

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References

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