Genetic Evidence of Causal Effect between C1q/TNF-Related Protein-1 and Atherosclerosis: a Bidirectional and Multivariate Mendelian Randomization Study

孟德尔随机化 多元统计 随机化 多元分析 内科学 医学 因果推理 孟德尔遗传 遗传变异 随机对照试验 生物信息学 遗传学 生物 基因 数学 统计 病理 基因型
作者
Juhong Pan,Jia Huang,Yueying Chen,Nan Jiang,Yuxin Guo,Ji Zhang,Shiyuan Zhou,Huan Pu,Qing Deng,Bo Hu,Qing Zhou
出处
期刊:Journal of Atherosclerosis and Thrombosis [Japan Atherosclerosis Society]
卷期号:32 (5): 630-648 被引量:1
标识
DOI:10.5551/jat.65313
摘要

AIMS: To investigate the causal relationship between C1q/TNF-related protein-1 (CTRP1) and atherosclerosis across various vascular sites, informed by studies connecting CTRP1 to coronary artery disease. METHODS: Summary statistics of CTRP1 from the available genome-wide association studies and atherosclerosis in classic vascular sites (including cerebral, coronary, and other arteries) from the FinnGen biobank were extracted for a primary MR analysis, and the analysis was replicated using Ischemic Stroke cohort (large artery atherosclerosis) for validation. The inverse variance-weighted method was used for primary assessment. Sensitivity analysis was performed by Cochrane's Q test and leave-one-out analysis. Potential pleiotropic effects were assessed by MR-Egger intercept and MR-PRESSO global test. Additionally, multivariable MR (MVMR) analysis was performed to investigate the independent effect of CTRP1 on atherosclerosis after removing confounding factors. RESULTS: Reliable causal evidence was found for CTRP1 involvement in three atherosclerosis endpoints: causal effects of CTRP1 on cerebral atherosclerosis (OR=1.31, CI:1.04-1.66; FDR_P=0.0222)], coronary atherosclerosis (OR=1.13, CI: 1.08-1.19; FDR_P=2.86e-07), and atherosclerosis at other sites (OR=1.06, CI:1.02-1.11; FDR_P=0.0125). The validation cohort further confirmed its causal effect on large-artery atherosclerosis (OR=1.10, CI:1.03-1.18; FDR_P=0.0115). The reverse MR analysis did not support the causal effect of atherosclerosis on CTRP1. Moreover, the MVMR analysis, adjusting for confounders (CTRP3, CTRP5, and CTRP9A), highlighted a significant independent causal effect of CTRP1 remaining on atherosclerosis. CONCLUSION: CTRP1 may represent a promising target for preventing and treating systemic atherosclerosis.

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