ArticleTranslational andrology and urology2024
A Mendelian randomization study on associations between plasma lipidome, circulating inflammatory proteins, and erectile dysfunction.
Article in Translational andrology and urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Mechanisms of dyslipidemia-induced erectile dysfunction: a narrative review.Frontiers in endocrinology · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Some studies suggest a potential association between plasma lipidome and erectile dysfunction (ED), but the underlying mechanism and whether circulating inflammatory proteins act as mediators remain unclear. The purpose of this study was to investigate the potential causal relationships between plasma lipidome, inflammatory proteins, and ED. Methods: Plasma lipidome, circulating inflammatory proteins, and ED cases were identified based on the summary data from several large-scale genome-wide association studies (GWAS). The causal relationships of plasma lipidome and circulating inflammatory proteins with ED were explored by a bidirectional two-sample, two-sample Mendelian randomization (MR) method. The inverse variance weighted (IVW) method was used as the primary analytical method. MR-Egger and the weighted median (IVW) methods were utilized as supplementary analytical techniques. Sensitivity analyses including MR-Pleiotropy RESidual Sum and Outlier method (PRESSO), Cochran's Q test, and MR-Egger intercept test were conducted to address heterogeneity and horizontal pleiotropy. Results: Ceramide (d42:2) and triacylglycerol (56:3) were found to be associated with an increased risk of ED, while phosphatidylethanolamine (O-18:1_18:2) and phosphatidylinositol (18:1_18:1) were linked to a decreased risk of ED. Interleukin-1α (IL-1α), IL-7, IL-17C, and the tumor necrosis factor (TNF) receptor superfamily member 9 (TNFRSF9) positively affected ED. Conversely, leukemia inhibitory factor and urokinase-type plasminogen activator (uPA) showed a negative impact. Mediation analysis indicated that the uPA mediated between Triacylglycerol (56:3) and ED, accounting for a mediation proportion of -14.71%. Conclusions: There was a causal relationship between plasma lipidome and circulating inflammatory proteins with ED. Circulating inflammatory proteins appeared to mediate between triacylglycerol (56:3) levels and ED.
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