ArticleFrontiers in medicine2025
Exploring the role of febuxostat's drug target XOR in erectile dysfunction: insights from human genetics and rat models.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The use of the uric acid-lowering drug Febuxostat (FB) has been associated with the risk of erectile dysfunction (ED) in men; however, findings from previous studies remain inconsistent. This study aimed to investigate the association between FB target genes and ED, as well as the underlying mechanisms involved. Methods: FB target genes were obtained from the DrugBank database. Mendelian randomization (MR) analysis was employed to determine the causal relationship between the target gene xanthine oxidoreductase (XOR) and ED. Molecular docking was then performed to assess the binding affinity between FB and XOR. A hyperuricemic rat model with ED was established, and several parameters were evaluated, including ICPmax/MAP ratio, serum testosterone, XOR, and p-eNOS/eNOS expression levels. In addition, levels of nitric oxide (NO), superoxide dismutase (SOD), malondialdehyde (MDA), and apoptosis in corpus cavernosum tissue were measured. Results: MR analysis revealed that XOR was significantly associated with an increased risk of ED (95% CI: 2.724-27.232; Conclusion: FB reducing oxidative stress and apoptosis in penile corpus cavernosum tissue in hyperuricemic rats by inhibiting XOR, thereby ameliorates 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.