Evidence map›Paper›PMID 41078899›Full record

ArticleArchives of medical science : AMS2025

The causal effects of placental weight on atherosclerotic cardiovascular disease: a Mendelian randomization and mediation analysis.

Dongyue Chen, Jiaxuan Sun, Shilin Fan, Chong Hou, Ke Yang, Min Peng, Songtao Shou, Quanyan Liu

Abstract read
In one paragraph

Article in Archives of medical science : AMS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Dongyue ChenDepartment of Hepatobiliary Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Jiaxuan SunDepartment of Emergency, Tianjin Medical University General Hospital, Tianjin, China.
Shilin FanDepartment of Critical Care Medicine, Tianjin Medical University General Hospital, Tianjin, China.
Chong HouDepartment of Emergency, Tianjin Medical University General Hospital, Tianjin, China.
Ke YangDepartment of Critical Care Medicine, Tianjin Medical University General Hospital, Tianjin, China.
Min PengDepartment of Critical Care Medicine, Tianjin Medical University General Hospital, Tianjin, China.
Songtao ShouDepartment of Emergency, Tianjin Medical University General Hospital, Tianjin, China.
Quanyan LiuDepartment of Hepatobiliary Surgery, Tianjin Medical University General Hospital, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

atherosclerotic cardiovascular diseasecoronary heart diseaseischemic strokemediation analysisMendelian randomizationplacental weight

Identifiers

PMID41078899
PMCPMC12509873

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.