ArticleBone reports2026
Bone transcriptomics reveals that juzentaihoto remodels and activates multiple pathways in Klotho-deficient mice.
Article in Bone reports, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Aging-related osteoporosis arises from an imbalance between bone formation and resorption. The traditional Japanese Kampo formula juzentaihoto (JTT) is used in the clinic to improve imbalances in systemic homeostasis, especially in elderly individuals; however, its effects on age-associated bone loss remain unclear. Here, we confirmed the effect of JTT on the osteoporotic phenotype in a model of aging, and explored its underlying mechanisms through transcriptomic analysis. Methods: Klotho-deficient mice, which have a shortened lifespan and display an aging-like phenotype that includes osteoporosis, were analyzed. Femoral bone mineral density (BMD) and cortical parameters were assessed by micro-computed tomography. RNA sequencing of femoral tissue was performed to identify differentially expressed genes in response to JTT administration, followed by Gene Ontology analysis and validation by RT-qPCR. Results: JTT treatment attenuated the decreased in BMD and cortical bone mass and increased cortical void volume, suggesting the potentially reflecting a reactivation of bone remodeling. Consistent with these findings, JTT restored the expression of genes involved in collagen biosynthesis, osteoblast differentiation, mineralization, and transcription factor NFATc1-centered osteoclast maturation. JTT also attenuated aberrant neurotransmitter-related signaling and induced the expression of genes encoding antioxidant enzymes, suggesting additional supportive effects on skeletal homeostasis. These changes occurred without recovery of the Klotho-fibroblast growth factor 23 (FGF23) or vitamin D pathways. Conclusions: JTT ameliorates low-turnover osteoporosis in Klotho-deficient mice by modulating multiple regulatory pathways that collectively promote bone remodeling. These multitarget actions highlight the therapeutic potential of JTT for age-related bone fragility and other conditions characterized by impaired bone formation.
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.