基于两样本孟德尔随机化分析脂质体与原发性高血压的因果关系

doi:10.3969/j.issn.1674-8115.2026.03.008

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (3): 340-347.doi: 10.3969/j.issn.1674-8115.2026.03.008

• 论著 · 循证医学 • 上一篇

基于两样本孟德尔随机化分析脂质体与原发性高血压的因果关系

黄玺¹, 侯钦午¹, 张兆伟¹, 王亚南¹, 杨庆辉²(), 程玲³

^1.上海市浦东新区北蔡社区卫生服务中心全科，上海 201204
^2.同济大学附属东方医院心血管内科，上海 200120
^3.同济大学附属东方医院中医针灸科，上海 200120

收稿日期:2025-09-12 接受日期:2025-12-05 出版日期:2026-03-28 发布日期:2026-03-30
通讯作者: 杨庆辉，主任医师，博士；电子信箱：qinghuiyang@tongji.edu.cn。
基金资助:
上海市浦东新区科技发展基金事业单位民生科研专项医疗卫生项目(PKJ2024-Y64);上海市浦东新区卫生健康委员会项目(PWZzk2022-25);上海市浦东新区卫生健康委员会项目(YC-2023-0612,PWYq2025-01)

Causal relationship between liposome and essential hypertension based on two-sample Mendelian randomization analysis

Huang Xi¹, Hou Qinwu¹, Zhang Zhaowei¹, Wang Yanan¹, Yang Qinghui²(), Cheng Ling³

^1.General Practice Department, Beicai Community Health Service Center, Pudong New Area, Shanghai 201204, China
^2.Department of Cardiology, East Hospital, Tongji University, Shanghai 200120, China
^3.Department of Traditional Chinese Medicine Acupuncture and Moxibustion, East Hospital, Tongji University, Shanghai 200120, China

Received:2025-09-12 Accepted:2025-12-05 Online:2026-03-28 Published:2026-03-30
Contact: Yang Qinghui, E-mail: qinghuiyang@tongji.edu.cn.
Supported by:
Medical and Health Project of the Special Fund for People′s Livelihood Scientific Research in Public Institutions under the Science and Technology Development Fund of Pudong New Area, Shanghai(PKJ2024-Y64);Project of the Health Commission of Pudong New Area, Shanghai(PWZzk2022-25)

摘要/Abstract

摘要：

目的·采用两样本孟德尔随机化（two-sample Mendelian randomization，TSMR）方法分析脂质体与原发性高血压的因果关系。方法·原发性高血压的全基因组关联分析（genome-wide association study，GWAS）数据来自FinnGen数据库，脂质体数据来自欧洲生物信息学研究所（European Bioinformatics Institute，EBI）。从EBI的GWAS数据库下载179种脂质体数据，并筛选相关的单核苷酸多态性（single-nucleotide polymorphism，SNP）作为工具变量。采用逆方差加权法（inverse-variance weighted，IVW）、MR-Egger回归、加权中位数法、加权模式法和简单模式法结合敏感性分析，综合评估179种脂质体与原发性高血压之间的因果关联。结果·共筛选出8种与原发性高血压相关的脂质体。IVW显示，6种脂质体增加原发性高血压风险，分别为甘油三酯（52∶3）（OR=1.061，95%CI 1.022~1.101，P=0.002），磷脂酰肌醇（16∶0-18∶1）（OR=1.066，95%CI 1.025~1.107，P=0.001），甘油三酯（50∶2）（OR=1.086，95%CI 1.036~1.139，P<0.001），甘油三酯（54∶3）（OR=1.062，95%CI 1.027~1.099，P<0.001），甘油三酯（50∶1）（OR=1.098，95%CI 1.045~1.154，P<0.001）和甘油三酯（52∶2）（OR=1.071，95%CI 1.035~1.110，P<0.001）。2种脂质体减少原发性高血压风险，分别为鞘磷脂（d40∶2）（OR=0.968，95%CI 0.937~0.999，P=0.042）和磷脂酰胆碱（O-16∶1-18∶1）（OR=0.960，95%CI 0.924~0.998，P=0.038）。其他4种方法显示的因果方向与IVW一致。Cochran′s Q检验显示存在轻微异质性，但对整体结果的稳健性影响有限。MR-Egger回归表明不存在水平多效性。留一法检验表明结果具有较高的稳健性。反向MR分析显示，原发性高血压发病不改变上述脂质体的类型。结论·特定脂质体与原发性高血压存在因果关联。甘油三酯（52∶3、50∶2、54∶3、50∶1、52∶2）和磷脂酰肌醇（16∶0-18∶1）是原发性高血压的危险因素，它们可能通过代谢紊乱促进原发性高血压发生。而鞘磷脂（d40∶2）和磷脂酰胆碱（O-16∶1-18∶1）或对原发性高血压的发生具有保护作用。

关键词: 脂质体, 原发性高血压, 孟德尔随机化, 因果关系

Abstract:

Objective ·A two-sample Mendelian randomization (TSMR) approach was employed to investigate the causal relationship between liposomes and essential hypertension. Methods ·Genome-wide association study (GWAS) data for essential hypertension were obtained from the FinnGen database, while lipid profile data were sourced from the European Bioinformatics Institute (EBI). Data on 179 liposomes were downloaded from the EBI GWAS database, and relevant single-nucleotide polymorphisms (SNPs) were screened as instrumental variables. Inverse-variance weighted (IVW), MR-Egger, weighted median, weighted mode, and simple mode methods, combined with sensitivity analysis, were employed to evaluate the causal associations between the 179 liposomes and essential hypertension. Results ·Eight types of liposomes were identified as being associated with essential hypertension. According to the IVW results, six types of liposomes significantly increased the risk of essential hypertension, including triglyceride (52:3) (OR=1.061, 95%CI 1.022‒1.101, P=0.002), phosphatidylinositol (16:0‒18:1) (OR=1.066, 95%CI 1.025‒1.107, P=0.001), triglyceride (50:2) (OR=1.086, 95%CI 1.036‒1.139, P<0.001), triglyceride (54:3) (OR=1.062, 95%CI 1.027‒1.099, P<0.001), triglyceride (50:1) (OR=1.098, 95%CI 1.045‒1.154, P<0.001), and triglyceride (52:2) (OR=1.071, 95%CI 1.035‒1.110, P<0.001). Two types of liposome reduced the risk of essential hypertension, including sphingomyelin (d40:2) (OR=0.968, 95%CI 0.937‒0.999, P=0.042) and phosphatidylcholine (O-16:1‒18:1) (OR=0.960, 95%CI 0.924‒0.998, P=0.038). The causal directions revealed by the other four methods were consistent with those of the IVW method. Cochran′s Q test revealed slight heterogeneity, but its impact on the robustness of the overall results was limited. MR-Egger regression indicated no evidence of horizontal pleiotropy. Leave-one-out cross-validation demonstrated high robustness of the results. Reverse MR analysis indicated that the onset of essential hypertension did not alter the type of the aforementioned liposomes. Conclusion ·There is a causal relationship between specific liposomes and essential hypertension. Triglycerides (52:3, 50:2, 54:3, 50:1, 52:2) and phosphatidylinositol (16:0‒18:1) are risk factors for essential hypertension, which may promote hypertension development through metabolic disturbances. Moreover, sphingomyelin (D40:2) and phosphatidylcholine (O-16:1‒18:1) may have protective effects against the occurrence of essential hypertension.

Key words: liposome, essential hypertension, Mendelian randomization (MR), causal relationship

中图分类号:

R544.1

黄玺, 侯钦午, 张兆伟, 王亚南, 杨庆辉, 程玲. 基于两样本孟德尔随机化分析脂质体与原发性高血压的因果关系[J]. 上海交通大学学报（医学版）, 2026, 46(3): 340-347.

Huang Xi, Hou Qinwu, Zhang Zhaowei, Wang Yanan, Yang Qinghui, Cheng Ling. Causal relationship between liposome and essential hypertension based on two-sample Mendelian randomization analysis[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026, 46(3): 340-347.

图/表 4

图1 脂质体与原发性高血压因果关系的森林图

Fig 1 Forest plot of the causal associations between liposomes and essential hypertension

图2 脂质体与原发性高血压相关性的散点图Note： A—F. Triglyceride (52:3) (A), phosphatidylinositol (16:0-18:1) (B), triglyceride (50:2) (C), triglyceride (54:3) (D), triglyceride (50:1) (E), and triglyceride (52:2) (F) were positively correlated with essential hypertension. G/H. Sphingomyelin (d40:2) (G) and phosphatidylcholine (O-16:1-18:1) (H) were negatively correlated with essential hypertension.

Fig 2 Scatter plot of the associations between liposomes and essential hypertension

表1 脂质体的多效性和异质性

Tab 1 Pleiotropy and heterogeneity of liposomes

Exposure factor	Variable	Pleiotropy			Heterogeneity
Exposure factor	Variable	Intercept	Standard error	P value	Method	Cochran Q	P value
Triglyceride (52:3)	Essential hypertension	0	0.006	0.942	IVW	103.532	<0.001
Phosphatidylinositl (16:0-18:1)	Essential hypertension	0.003	0.006	0.644	IVW	31.954	0.015
Triglyceride (50:2)	Essential hypertension	0.005	0.007	0.543	IVW	55.111	<0.001
Triglyceride (54:3)	Essential hypertension	0.004	0.005	0.418	IVW	82.530	<0.001
Triglyceride (50:1)	Essential hypertension	0.006	0.007	0.391	IVW	113.066	<0.001
Triglyceride (52:2)	Essential hypertension	0.004	0.006	0.470	IVW	53.829	<0.001
Sphingomyelin (d40:2)	Essential hypertension	-0.007	0.005	0.140	IVW	110.019	<0.001
Phosphatidylcholine (O-16:1-18:1)	Essential hypertension	0.001	0.007	0.887	IVW	5.067	<0.001

图3 脂质体与原发性高血压相关性的留一法分析结果

Fig 3 Leave-one-out sensitivity analysis of the associations between liposomes and essential hypertension

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基于两样本孟德尔随机化分析脂质体与原发性高血压的因果关系

Causal relationship between liposome and essential hypertension based on two-sample Mendelian randomization analysis

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