ArticleFrontiers in public health2025
Identification of a key environment-responsive gene mediating environmental impact on postmenopausal osteoporosis.
Article in Frontiers in public health, 2025. 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Osteoporosis is a multifactorial disease influenced by genetic, environmental, and metabolic factors. AKT serine/threonine kinase 1 (AKT1), a central regulator of cellular survival and metabolism, has been implicated in bone remodeling, yet its precise role in osteoporosis remains unclear. Methodology: Gene expression analysis and molecular docking simulations were performed to identify key pathways and interactions involving bisphenol A (BPA) and AKT1. Molecular dynamics simulations further assessed the stability of BPA-AKT1 binding. Experimental validation was conducted using bone marrow-derived macrophages (BMMs) treated with BPA. Osteoclastogenesis was evaluated through TRAcP staining, and AKT1 expression was analyzed via real-time PCR. Protein-level validation of AKT1 phosphorylation was performed using Western blot analysis to confirm its activation during osteoclast differentiation. Results: Computational analyses identified AKT1 as a key mediator linking BPA exposure to bone remodeling pathways. Molecular docking revealed strong interactions between BPA and AKT1, supported by molecular dynamics simulations showing stable binding. Experimental assays demonstrated that BPA significantly enhanced RANKL-mediated osteoclastogenesis, upregulated AKT1 mRNA expression, and promoted AKT1 phosphorylation. These findings indicate that BPA promotes bone resorption through AKT1 activation, potentially contributing to osteoporosis pathogenesis. Conclusion: AKT1 emerges as a critical node connecting environmental pollutants like BPA to bone health, highlighting its potential as a therapeutic target. These findings underscore the complexity of osteoporosis pathophysiology and the importance of mitigating environmental pollutant exposure.
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.