ArticleAMB Express2026
Multi-omics and mendelian randomization uncover microbial-metabolite-gene interactions in age-related hearing loss.
Article in AMB Express, 2026. 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
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
1 citing paper in PubMed.
- The Gut-Ear Axis: From Dysbiosis to Auditory and Vestibular Disorders.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related hearing loss (ARHL), as one of the most common sensory impairments among the elderly, has a complex etiology and lacks effective targeted intervention strategies. Through integrated multiomics analysis, we identified 38 ARHL core-associated candidate genes that are predominantly enriched in pathways such as NF-κB signaling, antigen presentation, and oxidative phosphorylation. These findings suggest potential metabolic dysregulation and features consistent with "inflammatory aging" in the cochlea. Mendelian randomization analysis further highlighted UROS, C1QB, and GLIPR1 as potential biomarkers with high predictive value (AUC 0.948-0.970) within our dataset. Analysis of immune infiltration revealed a positive association between GLIPR1 and Th2 and neutrophil expression. Through correlation analysis and GutMgene database screening, we observed that FPR2 and GLIPR1 are significantly co-expressed. Molecular docking and molecular dynamics simulations further suggested that FPR2 can bind to taurodeoxycholic acid with high stability. Based on these findings, we hypothesize the existence of a "Roseburia-FPR2-taurodeoxycholic acid" regulatory network that may contribute to ARHL. This speculative model provides a novel framework for future investigations into the potential role of the gut-inner ear axis in ARHL.
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.