ArticleJCI insight2025
Inhibition of AhR improves cortical bone and skeletal muscle function via preservation of neuromuscular junctions.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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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.
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Who cites it
8 citing papers in PubMed.
- Mechanistic Insights into Regulation of the Aryl Hydrocarbon Receptor Expression in Mouse and Human Hepatoma Cells.International journal of molecular sciences · 2026Article
- Review
- Article
- The Integration of Bioinformatics with Experimental Validation Has Uncovered Shared Molecular Characteristics Between Sarcopenia and Osteoarthritis.Calcified tissue international · 2026Article
- Microbiota-derived indole-3-propionic acid extends lifespan in Drosophila and improves muscle and bone health in mice.GeroScience · 2026Article
- Sea buckthorn berry extract favorably affects bone metabolism-related biomarkers and collagen deposition in cultured rat primary osteoblasts.Open life sciences · 2026Article
- The gut-bone axis: mechanisms through which oleic acid regulates bone metabolism and its potential in preventing and treating osteoporosis.Frontiers in nutrition · 2026Review
- Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies.Research (Washington, D.C.) · 2026Review
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
The aryl hydrocarbon receptor (AhR) is proposed to mediate the frailty-promoting effects of the tryptophan metabolite kynurenine, which increases with age in mice and humans. The goal of the current study was to test whether administration of pharmacological AhR inhibitors, BAY2416964 and CH-223191, could abrogate musculoskeletal decline in aging mice. Female C57BL/6 mice (18 months old) were treated with vehicle (VEH) or 30 mg/kg BAY2416964 (BAY) via daily oral gavage 5 days/week for 8 weeks. A second AhR antagonist, CH-223191, was administered to 16-month-old male and female C57BL/6 mice via intraperitoneal injections (3.3 mg/kg) 3 days/week for 12 weeks. While grip strength declined over time in VEH-treated mice, BAY preserved grip strength in part by improving integrity of neuromuscular junctions (NMJs), an effect replicated during in vitro studies with siRNA against AhR. Cortical bone mass was also greater in BAY- than VEH-treated mice. Similarly, CH-223191 treatment improved cortical bone and showed beneficial effects in skeletal muscle, including reducing oxidative stress as compared with VEH-treated animals. Transcriptomic and proteomic data from BAY-treated mice supported a positive impact of BAY on molecular targets that affect NMJ function. Taken together, these data support AhR as a therapeutic target for improving musculoskeletal health during aging.
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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.