ArticleLipids in health and disease2024
Causal and mediating effects of lipid and facial aging: association study integrating GWAS, eQTL, mQTL, and pQTL data.
Article in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- Unraveling the role of lipid metabolism in polycystic ovary syndrome through multi-omics Mendelian randomization.Journal of ovarian research · 2026Article
- Multi-omics Mendelian randomization and machine learning identify candidate therapeutic targets for Alzheimer's and Parkinson's diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Genetically Proxied Biological Aging and Risk of Hypertrophic Scar/Keloid-Coded Phenotypes: An Exploratory Two-Sample Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- PSMA4 as a Druggable Target in Hidradenitis Suppurativa: Evidence From Mendelian Randomization and Single-Cell Transcriptomics.Mediators of inflammation · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundIncreasing evidence suggests a potential causal association between lipid levels and facial aging. The aim of this study was to investigate the relationship between levels of specific lipids and facial aging via Mendelian randomization methods. Additionally, this study aimed to identify mediators and explore relevant genes and drug targets.
methodsIn this study, genome-wide association data on plasma lipids from 7,174 Finnish individuals in the UK Biobank were used. Two-sample Mendelian randomization was applied to assess the causal effects of specific lipids on facial aging. Sensitivity and pleiotropy analyses were conducted to ensure the robustness and reliability of the results. Multivariate Mendelian randomization was conducted to account for the potential impact of confounding factors. Furthermore, summary-data-based Mendelian randomization was used to identify relevant genes, which were validated through multiomics data. Finally, drug‒gene interactions were explored via molecular docking techniques.
resultsTwo-sample Mendelian randomization analysis revealed a causal relationship between lipid levels and facial aging. According to the multivariate Mendelian randomization results, smoking was found to mediate this association, and these lipids remained significantly associated with facial aging, even after accounting for environmental confounders. Using summary-data-based Mendelian randomization, CYP21A2, CCND1, PSMA4, and MED1 were identified as potential gene targets, with MED1 further validated through pQTL and mQTL data. Additionally, the MED1 protein was found to bind spontaneously with astragalin, fenofibrate, and ginsenoside.
conclusionsThe results revealed a causal relationship between lipid levels and facial aging, revealing key gene targets that were still significantly associated with facial aging after controlling for environmental confounders. Additionally, the interactions between MED1 and certain drugs may indicate potential pathways for therapeutic interventions related to facial aging.
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