Exploring Causal Correlations Between Inflammatory Cytokines and Kawasaki Disease: A Mendelian Randomization.

IF 0.7 4区 医学 Q4 PATHOLOGY Fetal and Pediatric Pathology Pub Date : 2024-11-01 DOI:10.1080/15513815.2024.2414175
Yan Pan, Fuyong Jiao
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引用次数: 0

Abstract

Background: The role of inflammatory cytokines in Kawasaki disease (KD) pathogenesis is known, but causal relationships are unclear. This study investigates these connections using Mendelian randomization (MR).

Methods: Genetic variations associated with KD were obtained from a GWAS including 119 cases and 6071 controls of European ancestry. Genetic data on inflammatory cytokines were sourced from a GWAS of 8,293 healthy participants.

Results: The study identified significant associations between higher levels of macrophage colony stimulating factor (M-CSF), monocyte chemotactic protein-1 (MCP-1), and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and increased risk of KD. The odds ratios (OR) were 1.04 (95% CI: 1.01-1.08, p = 0.010) for M-CSF, 1.03 (95% CI: 1.01-1.05, p = 0.026) for MCP-1, and 1.02 (95% CI: 1.01-1.04, p = 0.027) for TRAIL.

Conclusion: This study suggests that M-CSF, MCP-1, and TRAIL are potentially involved in the etiology of KD.

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探索炎症细胞因子与川崎病之间的因果关系:孟德尔随机试验
背景:已知炎性细胞因子在川崎病(KD)发病机制中的作用,但其因果关系尚不清楚。本研究采用孟德尔随机化方法(MR)调查了这些关系:与 KD 相关的遗传变异来自一项全球基因组研究,其中包括 119 例病例和 6071 例欧洲血统对照。有关炎症细胞因子的遗传数据来自一项针对 8293 名健康参与者的基因组研究:研究发现,巨噬细胞集落刺激因子(M-CSF)、单核细胞趋化蛋白-1(MCP-1)和肿瘤坏死因子相关凋亡诱导配体(TRAIL)水平较高与 KD 风险增加之间存在明显关联。M-CSF的几率比(OR)为1.04(95% CI:1.01-1.08,P = 0.010),MCP-1的几率比(OR)为1.03(95% CI:1.01-1.05,P = 0.026),TRAIL的几率比(OR)为1.02(95% CI:1.01-1.04,P = 0.027):本研究表明,M-CSF、MCP-1和TRAIL可能与KD的病因有关。
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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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