Dongyue Chen, Jiaxuan Sun, Shilin Fan, Chong Hou, Ke Yang, Min Peng, Songtao Shou, Quanyan Liu
{"title":"胎盘重量对动脉粥样硬化性心血管疾病的因果影响：孟德尔随机化和中介分析","authors":"Dongyue Chen, Jiaxuan Sun, Shilin Fan, Chong Hou, Ke Yang, Min Peng, Songtao Shou, Quanyan Liu","doi":"10.5114/aoms/194244","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Previous studies have linked placental weight (PW) to cardiovascular diseases, but the causality and potential mediators underlying this relationship are still unknown.</p><p><strong>Material and methods: </strong>We conducted Mendelian randomization (MR) analysis via summary statistics from genome-wide association studies (GWAS), including PW adjusted for sex, 21 candidate mediators and atherosclerotic cardiovascular disease (ASCVD), which includes coronary heart disease (CHD) and ischemic stroke (IS). Two-step MR was employed to identify and assess the mediation and proportion of potential mediators in the association between PW and ASCVD. Additionally, we conducted a repeated analysis using PW adjusted for gestational age and sex.</p><p><strong>Results: </strong>Univariable MR (UVMR) analysis revealed that for each 1-SD decrease in fetal genotype-determined PW adjusted for sex only, the risk of CHD increased by 24% (95% CI: 1.05-1.46) and the risk of large artery stroke (LAS) increased by 46% (95% CI: 1.13-1.89). Similar results were obtained in repeated analyses. The mediation MR analysis revealed that the causal relationship between fetal genotype-determined PW and CHD risk was primarily mediated by birthweight, type 2 diabetes, and education, each mediating 3.66% to 40.80% of the total effect. The causal relationship between fetal genotype-determined PW and LAS risk was mediated mainly by type 2 diabetes, which accounted for 22.11% of the total effect.</p><p><strong>Conclusions: </strong>This study identified a unidirectional causal relationship between lower PW and a greater ASCVD risk, with factors such as birthweight, type 2 diabetes, and education mediating the association between PW and ASCVD.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"21 4","pages":"1141-1151"},"PeriodicalIF":3.3000,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12509873/pdf/","citationCount":"0","resultStr":"{\"title\":\"The causal effects of placental weight on atherosclerotic cardiovascular disease: a Mendelian randomization and mediation analysis.\",\"authors\":\"Dongyue Chen, Jiaxuan Sun, Shilin Fan, Chong Hou, Ke Yang, Min Peng, Songtao Shou, Quanyan Liu\",\"doi\":\"10.5114/aoms/194244\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Previous studies have linked placental weight (PW) to cardiovascular diseases, but the causality and potential mediators underlying this relationship are still unknown.</p><p><strong>Material and methods: </strong>We conducted Mendelian randomization (MR) analysis via summary statistics from genome-wide association studies (GWAS), including PW adjusted for sex, 21 candidate mediators and atherosclerotic cardiovascular disease (ASCVD), which includes coronary heart disease (CHD) and ischemic stroke (IS). Two-step MR was employed to identify and assess the mediation and proportion of potential mediators in the association between PW and ASCVD. Additionally, we conducted a repeated analysis using PW adjusted for gestational age and sex.</p><p><strong>Results: </strong>Univariable MR (UVMR) analysis revealed that for each 1-SD decrease in fetal genotype-determined PW adjusted for sex only, the risk of CHD increased by 24% (95% CI: 1.05-1.46) and the risk of large artery stroke (LAS) increased by 46% (95% CI: 1.13-1.89). Similar results were obtained in repeated analyses. The mediation MR analysis revealed that the causal relationship between fetal genotype-determined PW and CHD risk was primarily mediated by birthweight, type 2 diabetes, and education, each mediating 3.66% to 40.80% of the total effect. The causal relationship between fetal genotype-determined PW and LAS risk was mediated mainly by type 2 diabetes, which accounted for 22.11% of the total effect.</p><p><strong>Conclusions: </strong>This study identified a unidirectional causal relationship between lower PW and a greater ASCVD risk, with factors such as birthweight, type 2 diabetes, and education mediating the association between PW and ASCVD.</p>\",\"PeriodicalId\":8278,\"journal\":{\"name\":\"Archives of Medical Science\",\"volume\":\"21 4\",\"pages\":\"1141-1151\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2024-10-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12509873/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archives of Medical Science\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5114/aoms/194244\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Medical Science","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5114/aoms/194244","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
The causal effects of placental weight on atherosclerotic cardiovascular disease: a Mendelian randomization and mediation analysis.
Introduction: Previous studies have linked placental weight (PW) to cardiovascular diseases, but the causality and potential mediators underlying this relationship are still unknown.
Material and methods: We conducted Mendelian randomization (MR) analysis via summary statistics from genome-wide association studies (GWAS), including PW adjusted for sex, 21 candidate mediators and atherosclerotic cardiovascular disease (ASCVD), which includes coronary heart disease (CHD) and ischemic stroke (IS). Two-step MR was employed to identify and assess the mediation and proportion of potential mediators in the association between PW and ASCVD. Additionally, we conducted a repeated analysis using PW adjusted for gestational age and sex.
Results: Univariable MR (UVMR) analysis revealed that for each 1-SD decrease in fetal genotype-determined PW adjusted for sex only, the risk of CHD increased by 24% (95% CI: 1.05-1.46) and the risk of large artery stroke (LAS) increased by 46% (95% CI: 1.13-1.89). Similar results were obtained in repeated analyses. The mediation MR analysis revealed that the causal relationship between fetal genotype-determined PW and CHD risk was primarily mediated by birthweight, type 2 diabetes, and education, each mediating 3.66% to 40.80% of the total effect. The causal relationship between fetal genotype-determined PW and LAS risk was mediated mainly by type 2 diabetes, which accounted for 22.11% of the total effect.
Conclusions: This study identified a unidirectional causal relationship between lower PW and a greater ASCVD risk, with factors such as birthweight, type 2 diabetes, and education mediating the association between PW and ASCVD.
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