ArticleJournal of orthopaedic translation2026
Ganoderic acid A accelerates osteoporotic fracture healing by promoting osteogenic differentiation via estrogen receptor alpha binding.
Article in Journal of orthopaedic translation, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Ganoderic acid A (GAA), a natural triterpenoid derived from the fungal species Methods: An ovariectomized femoral fracture model was treated with GAA or estradiol benzoate. Callus formation, mineralization and bone mineral density (BMD) were assessed by micro-computed tomography, radiographic scoring and DXA. Mechanical properties were evaluated by three-point bending tests. Histological analyses and enzyme-linked immunosorbent assay for serum bone formation and resorption markers were performed. RNA sequencing with GO, KEGG and GSEA analyses was used to explore molecular mechanisms. In vitro, MC3T3-E1 cells were used to assess osteogenic differentiation under GAA, estrogen receptor (ER) antagonist (ICI 182780) or selective ERα antagonist (Methyl-piperidino-pyrazole dihydrochloride, MPP) treatment. Biophysical interaction assays and molecular simulations were employed to characterize GAA-ERα interactions. Results: GAA enhanced early callus mineralization, bone volume fraction, callus volume and trabecular number, and increased radiographic union, bone mineral density and flexural rigidity in OF mice. Histological analysis showed increased soft callus and mineralized bone with elevated bone formation and resorption markers. Transcriptomic analyses indicated that GAA modulated hormone-related pathways, identifying the estrogen signaling pathway as a key target. In vitro, GAA promoted alkaline phosphatase activity, mineral deposition and expressions of phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2), Runt-related transcription factor 2 (RUNX2) and bone morphogenetic protein 2 (BMP2), all of which were abrogated by ICI 182780 and MPP. Notably, molecular interaction studies demonstrated direct and stable binding of GAA to ERα. Conclusion: GAA promotes osteogenic differentiation and accelerates OF healing via ERα. The translational potential of this article: The work offers a conceptual advance by identifying a fungal-derived small molecule that functions as an ERα ligand to promote fracture repair, supporting its potential as a therapeutic candidate for OF.
Indexed as
Identifiers
What Socratic 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 Socratic graph.