ArticleHistology and histopathology2024
CBP-mediated FOXO4 acetylation facilitates postmenopausal osteoporosis (PMO) progression through the inhibition of the Wnt/β-catenin signaling pathway.
Article in Histology and histopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 0 citations in OpenAlex.
- SIRT7-mediated desuccinylation of FOXO4 suppresses ferroptosis to alleviate LPS-induced acute lung injury.Redox biology · 2026Article
- The Role of Wnt Signaling in Age-Related Alveolar Bone Loss and Regeneration.Journal of periodontal research · 2026Review
- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- Bidirectional regulation factor of bone marrow mesenchymal stromal cells differentiation: a focus on bone-fat balance in osteoporosis.Stem cell research & therapy · 2025Review
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
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Authors and funding
2 authors at 2 institutions in 1 country.
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Abstract
FOXO4 was previously identified as a potential biomarker and therapeutic target for postmenopausal osteoporosis (PMO) using bioinformatic analysis, but its specific function and molecular mechanism in the progression of osteoporosis was not reported. The current study was designed to investigate the biological function and underlying mechanism of FOXO4 in PMO. Our results showed that FOXO4 expression was significantly upregulated in the serum samples of PMO patients, which was also negatively correlated with the expression of osteogenesis genes (OCN and ALP). In addition, FOXO4 depletion alleviated osteoporosis by facilitating osteogenic differentiation and inhibiting adipogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs). Overexpression of FOXO4 exerted the opposite effects on the osteogenic/adipogenic differentiation in hBMSCs. Moreover, FOXO4 knockdown activated the Wnt/β-catenin signaling whereas the inhibition of Wnt/β-catenin signaling overturned the effects of FOXO4 deficiency on osteoporosis. Furthermore, FOXO4 upregulation in PMO was caused by CBP-induced acetylation. In summary, our data demonstrated that FOXO4 was a potent biomarker for PMO and mediated the balance between osteogenesis and adipogenesis in hBMSCs by regulating Wnt/β-catenin signaling.
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