ArticleMedicine2026
Multi-scale analysis reveals key targets mediating BPA-induced sensorineural hearing loss.
Article in Medicine, 2026. 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
3 authors.
Funding
Abstract
The mechanism of bisphenol A (BPA) on sensorineural hearing loss (SNHL) remains undefined. This study investigates BPA's toxic mechanism on SNHL. ProTox database was performed to analyze the toxicity of BPA. Intersection genes were screened using network toxicology, and causal genes associated with SNHL were identified through Mendelian randomization. The ligand-protein binding activity was validated through molecular docking and dynamic simulation. BPA showed a toxicity classification of Class 4, with toxicological profiles involving the blood-brain barrier, mitochondrial membrane potential, and estrogen receptor alpha. A total of 92 BPA target genes were found to be related to SNHL. These were enriched in potassium ion channel processes and MAPK, PI3K-Akt pathways. Two-sample Mendelian randomization identified 3 causal genes, with small effect sizes: MANBA (odds ratios [OR] = 0.950, P = .009), PDE6D (OR = 1.055, P = .001), vascular endothelial growth factor A (OR = 1.030, P = .022). Molecular docking with BPA revealed minimum binding free energies of -8.1, -6.7, and -6.1 kcal/mol; MANBA-BPA binding was stable in dynamics simulations. BPA can exert toxic effects on SNHL through potassium channel related processes, as well as MAPK and PI3K-Akt signaling pathways. MANBA, PDE6D, and vascular endothelial growth factor A also play key mediating roles in this process.
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.