ArticleDrug design, development and therapy2022
ED-71 Prevents Glucocorticoid-Induced Osteoporosis by Regulating Osteoblast Differentiation via Notch and Wnt/β-Catenin Pathways.
Article in Drug design, development and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Glycolysis in bone remodeling: from energy supply to signaling regulation.Molecular biology reports · 2026Review
- Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis.Bioactive materials · 2026Article
- Article
- Bakuchiol Ameliorates Glucocorticoid-Induced Osteoporosis by Enhancing Osteoblast Differentiation via Targeting FAT4 to Activate YAP1.Phytotherapy research : PTR · 2026Article
- Wubi Shanyao Pills ameliorate glucocorticoid-induced osteoporosis by regulating bone marrow T cell homing as an immune intermediate to restore bone metabolism.Chinese medicine · 2026Article
- Risperidone induces osteoporosis and neuropsychiatric treatment resistance via SMPD1-lysosome-mediated ferroptosis: dual rescue by active vitamin D analog ED-71.Journal of advanced research · 2026Article
- Bone-seeking nanomaterials for rebalancing bone remodeling in osteoporosis.International journal of pharmaceutics: X · 2026Review
- LNGFR promoting osteogenic differentiation of ectomesenchyme stem cells via activation of GHR-JAK-STAT/IGF1 signaling pathway.Stem cell research & therapy · 2026Article
- Identification of common genetic features and pathways for osteoporosis with frozen shoulder by integrated bioinformatics analysis and machine learning.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- DAPT Mitigates Osteoarthritic Cartilage Degeneration and Enhances Articular Repair Through Targeted Modulation of the Gucy1a3 and Notch Signaling Axis.Drug design, development and therapy · 2026Article
- Context-dependent roles of 11β-HSD1 in bone and skeletal muscle diseases.American journal of translational research · 2026Review
- A Cross-Tissue Multiomics Analysis Reveals the Protective Role of TGFBR3 in Postmenopausal Osteoporosis.International journal of genomics · 2026Article
- FOXJ3 drives mesenchymal stem cell osteogenic differentiation via the Wnt/β‑catenin pathway: A novel regulator implicated in osteoporosis.Molecular medicine reports · 2026Article
- The Notch signaling pathway in regulating bone and cartilage homeostasis: novel insights into the pathogenesis and therapeutics of osteoarthritis.Cell communication and signaling : CCS · 2025Review
- YS-49 activates the PI3K/AKT signaling pathway in MC3T3-E1 cells to enhance osteoblast differentiation and inhibits glucocorticoid-induced bone loss in vivo.BMC musculoskeletal disorders · 2025Article
- Isorhynchophylline Mitigates Bone Loss in OVX Mice by Modulating Inflammatory Responses, Oxidative Stress, Gut Microbiota Composition and SCFAs Production.Food science & nutrition · 2025Article
- Review
- Exploring the Mechanisms of Sanguinarine in the Treatment of Osteoporosis by Integrating Network Pharmacology Analysis and Deep Learning Technology.Current computer-aided drug design · 2025Article
- MK-4 Ameliorates Diabetic Osteoporosis in Angiogenesis-Dependent Bone Formation by Promoting Mitophagy in Endothelial Cells.Drug design, development and therapy · 2025Article
- Vitamin KDrug design, development and therapy · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Long-term glucocorticoid- usage can lead to glucocorticoid-induced osteoporosis (GIOP). The study focused on the preventative effects of a novel active vitamin D3 analog, eldecalcitol (ED-71), against GIOP and explored the underlying molecular mechanisms. Methods: Intraperitoneal injection of methylprednisolone (MPED) or dexamethasone (DEX) induced the GIOP model within C57BL/6 mice in vivo. Simultaneously, ED-71 was orally supplemented. Bone histological alterations, microstructure parameters, novel bone formation rates, and osteogenic factor changes were evaluated by hematoxylin-eosin (HE) staining, micro-computed tomography, calcein/tetracycline labeling, and immunohistochemical (IHC) staining. The osteogenic differentiation level and mineralization in pre-osteoblast MC3T3-E1 cells were evaluated in vitro using alkaline phosphatase (ALP) staining, alizarin red (AR) staining, quantitative polymerase chain reaction (qPCR), Western blotting, and immunofluorescence staining. Results: ED-71 partially prevented bone mass reduction and microstructure parameter alterations among GIOP-induced mice. Moreover, ED-71 also promoted new bone formation and osteoblast activity while inhibiting osteoclasts. In vitro, ED-71 promoted osteogenic differentiation and mineralization in DEX-treated MC3T3-E1 cells and boosted the levels of osteogenic-related factors. Additionally, GSK3-β and β-catenin expression levels were elevated after ED-71 was added to cells and were accompanied by reduced Notch expression. The Wnt signaling inhibitor XAV939 and Notch overexpression reversed the ED-71 promotional effects toward osteogenic differentiation and mineralization. Conclusion: ED-71 prevented GIOP by enhancing osteogenic differentiation through Notch and Wnt/GSK-3β/β-catenin signaling. The results provide a novel translational direction for the clinical application of ED-71 against GIOP.
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