ArticleJournal of cellular and molecular medicine2025
FKBP5 Induces Senescence in BMSCs and Inhibits Osteogenic Differentiation Through the Canonical WNT/β-Catenin Signalling Pathway in Senile Osteoporosis.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed.
- Age-related transcriptional drift and physiological adaptation in long-living Ames dwarf skeletal muscle.NAR molecular medicine · 2026Article
- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- TRIM27 Ubiquitinates and Degrades PPARγ to Promote Osteogenic Differentiation of BMSCs and Alleviate Osteoporosis.International journal of endocrinology · 2026Article
- The Role of Senolytics in Osteoporosis.Biomolecules · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Senile osteoporosis and its associated fractures significantly contribute to increased morbidity, mortality, and healthcare costs among older adults. Further research is needed to elucidate the molecular mechanisms underlying senile osteoporosis. This study found that FKBP5 expression in bone marrow mesenchymal stem cells (BMSCs) increases with age and is inversely correlated with patients' bone mineral density and CT values. Functional analyses revealed that FKBP5 plays a crucial regulatory role in BMSC osteogenic differentiation, acting through the canonical WNT/β-catenin signalling pathway. FKBP5 binds to β-catenin, promoting its ubiquitination and degradation. Importantly, administration of SAFit2, a selective FKBP5 inhibitor, enhanced bone mineral density in an animal model of senile osteoporosis. These findings suggest that FKBP5 may represent a novel therapeutic target and provide new insights into the treatment of senile osteoporosis.
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Registered trials
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