ArticleTranslational andrology and urology2024
Causal relationship between immune cells, inflammatory cytokines, metabolites, and erectile dysfunction: a two-sample Mendelian randomization study.
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 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Integrative analysis of mortality risk in SFTS using machine learning and genetic approaches.mSphere · 2026Article
- Association between the inflammatory burden index and erectile dysfunction: a cross-sectional study based on NHANES 2001-2004.Journal of health, population, and nutrition · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous studies have investigated the association between immune inflammation, metabolism and erectile dysfunction (ED). However, these studies are limited by biases, confounding factors, and reverse causality, failing to establish causality. We conducted a two-sample Mendelian randomization (MR) study to elucidate the causal relationships between immune cells, inflammatory cytokines, plasma metabolites, and the risk of ED. Methods: Data on 91 inflammatory cytokines (n=14,736), 731 immune phenotypes (n=3,757) and 1,400 circulating metabolites (n=8,000) were obtained from genome-wide association studies (GWAS) as exposures, while ED data were sourced from the Integrative Epidemiology Unit (IEU) Open GWAS database (n=223,805) as outcomes. A two-sample MR analysis was performed to determine the relationships between exposures and outcomes. The inverse variance weighted (IVW) method was used as the primary MR analysis approach, supplemented by additional methods. Sensitivity analyses, including Cochran's Q test for heterogeneity and MR-Egger intercept for horizontal pleiotropy, were conducted to assess the robustness of the MR results. Results: At a significance level of P<0.01, we identified 12 factors associated with ED: five immune cells, one inflammatory cytokine, two metabolites, and four metabolite ratios. Specifically, CD19 on immunoglobulin D- (IgD-) CD38+ B cells [odds ratio (OR) =1.17; 95% confidence interval (CI): 1.06-1.30], CD4 on terminally differentiated CD4+ T cells (OR =1.07; 95% CI: 1.02-1.12), CD25 on IgD+ CD38dim B cells (OR =1.05; 95% CI: 1.01-1.09), CD25 on IgD+ CD24- B cells (OR =1.04; 95% CI: 1.01-1.07), and IgD on IgD+ B cells (OR =0.88; 95% CI: 0.79-0.97) were associated with ED. Among inflammatory cytokines, only elevated levels of urokinase-type plasminogen activator (uPA) significantly reduced the risk of ED (OR =0.83; 95% CI: 0.73-0.95). Six metabolites, including glycerol levels (OR =1.30; 95% CI: 1.08-1.56), aspartate to N-acetylglucosamine to N-acetylgalactosamine ratio (OR =1.21; 95% CI: 1.07-1.37), cholesterol to taurocholate ratio (OR =1.23; 95% CI: 1.07-1.42), 4-methyl-2-oxopentanoate to 3-methyl-2-oxobutyrate ratio (OR =1.26; 95% CI: 1.07-1.48), alpha-ketoglutarate to kynurenine ratio (OR =0.86; 95% CI: 0.76-0.96), and X-16964 levels (OR =1.24; 95% CI: 1.06-1.45) were significantly associated with ED. Sensitivity analyses did not reveal any heterogeneity or pleiotropy. Conclusions: Our MR analysis indicates that immune inflammation and metabolism have both inducing and protective effects on ED risk. These findings provide new insights for clinicians regarding the treatment and prevention of ED. Additionally, our study offers novel insights into the pathogenesis of ED.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.