ArticleThe Journal of biological chemistry2026
Geranylgeraniol promotes osteoblast differentiation and inhibits osteoclastogenesis through MAPK and nuclear receptor signaling.
Article in The Journal of biological chemistry, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone is regulated in a coordinated manner through the catabolic action of osteoclasts and the anabolic function of osteoblasts. Geranylgeraniol (GGOH) is a diterpenoid alcohol found in plant oils and is an intermediate in the mevalonate pathway. GGOH suppressed receptor activator of NF-κB ligand (RANKL)-induced tartrate-resistant acid phosphatase-positive multinuclear osteoclast formation via downregulation of nuclear factor of activated T-cells cytoplasmic 1 expression. Among the RANKL-activated mitogen-activated protein kinases in bone marrow cells, phosphorylation of c-Jun amino-terminal kinase was significantly suppressed following GGOH treatment. In contrast, GGOH stimulates alkaline phosphatase (ALP) activity and mineralization in calvarial osteoblasts. GGOH increased the expression of osteoblast biomarkers such as collagen type 1 and ALP, and osteogenic genes, such as Msx2, Runx2, and Smad. Mitogen-activated protein kinase signaling pathway (c-Jun amino-terminal kinase, p38, extracellular signal-regulated kinase) and NF-κB were augmented by GGOH. GGOH-induced ALP expression was suppressed by a farnesoid X receptor (FXR) antagonist, whereas FXR agonist increased ALP activity in osteoblasts. In contrast, the suppressive effect of GGOH on RANKL-induced tartrate-resistant acid phosphatase activity in osteoclasts was attenuated by liver X receptor and FXR antagonists, and these agonists mimicked the effect of GGOH. GGOH restored bisphosphonate-suppressed osteoblast differentiation. GGOH also showed protective effects against lipopolysaccharide -induced bone resorption both in vitro and in vivo. Furthermore, GGOH treatment improved bone loss in ovariectomized mice. These results suggest that GGOH is a potent osteogenic and osteoprotective factor that promotes osteoblast differentiation and suppresses osteoclast differentiation, at least through nuclear receptor activation.
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.