ReviewTzu chi medical journal
The molecular etiology and treatment of glucocorticoid-induced osteoporosis.
Review in Tzu chi medical journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- The miR-212-3p/transferrin axis promotes bone regeneration by modulating iron homeostasis through Schwann cell Exosome-BMSCs communication.Bioactive materials · 2026Article
- Klotho Attenuates Glucocorticoid-Induced Osteoblast Cytotoxicity Via Wnt Signaling Pathway Modulation.Biochemical genetics · 2026Article
- Bone Health in Rheumatoid Arthritis: An Update.Current rheumatology reports · 2026Review
- Pathophysiology and Molecular Signalling in Osteoporosis: Linking Risk Factors to Bone Loss.Journal of cellular and molecular medicine · 2026Review
- Ascorbic Acid Modulates Collagen Properties in Glucocorticoid-Induced Osteoporotic Bone: Insights into Chemical, Mechanical, and Biological Regulation.Advanced healthcare materials · 2026Article
- Acid-Responsive Nanocarriers for Site-Specific Osteoclast Inhibition and Osteoporosis Therapy: A Review.International journal of nanomedicine · 2026Review
- Therapeutic functions of tanshinone IIA in a zebrafish model of glucocorticoid-induced osteoporosis.Frontiers in pharmacology · 2026Article
- High-efficient discovering the potent anti-Notum agents from herbal medicines for combating glucocorticoid-induced osteoporosis.Acta pharmaceutica Sinica. B · 2025Article
- Capsaicin counteracts dexamethasone-induced osteoporosis and metabolic disturbances in rats: role of AMPK/SIRT1/β-catenin/RUNX2 pathway.Journal of molecular histology · 2025Article
- PET/CT for the Opportunistic Screening of Osteoporosis and Fractures in Cancer Patients.Current osteoporosis reports · 2024Review
- Foliar spraying with zinc oxide nanoparticles enhances the anti-osteoporotic efficacy of the fruit extracts ofFrontiers in plant science · 2024Article
- Osteoporosis treatment: current drugs and future developments.Frontiers in pharmacology · 2024Review
- Metabolomics analysis of the potential mechanism of Yi-Guan-Jian decoction to reverse bone loss in glucocorticoid-induced osteoporosis.Journal of orthopaedic surgery and research · 2023Article
- Carbonic Anhydrase II Activators in Osteopetrosis Treatment: A Review.Current issues in molecular biology · 2023Review
- The effect of Rutin hydrate on Glucocorticoids induced osteoporosis in mandibular alveolar bone in Albino rats (Radiological, histological and histochemical study).The Saudi dental journal · 2022Article
- A bibliometric and visualization analysis of glucocorticoid-induced osteoporosis research from 2012 to 2021.Frontiers in endocrinology · 2022Article
- ED-71 Prevents Glucocorticoid-Induced Osteoporosis by Regulating Osteoblast Differentiation via Notch and Wnt/β-Catenin Pathways.Drug design, development and therapy · 2022Article
- Osteoporosis in Patients With Respiratory Diseases.Frontiers in physiology · 2022Review
- Expression of Renal Vitamin D and Phosphatonin-Related Genes in a Sheep Model of Osteoporosis.Animals : an open access journal from MDPI · 2021Article
- Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid-induced osteoporosis (GIOP) is the most common form of secondary osteoporosis, accounting for 20% of osteoporosis diagnoses. Using glucocorticoids for >6 months leads to osteoporosis in 50% of patients, resulting in an increased risk of fracture and death. Osteoblasts, osteocytes, and osteoclasts work together to maintain bone homeostasis. When bone formation and resorption are out of balance, abnormalities in bone structure or function may occur. Excess glucocorticoids disrupt the bone homeostasis by promoting osteoclast formation and prolonging osteoclasts' lifespan, leading to an increase in bone resorption. On the other hand, glucocorticoids inhibit osteoblasts' formation and facilitate apoptosis of osteoblasts and osteocytes, resulting in a reduction of bone formation. Several signaling pathways, signaling modulators, endocrines, and cytokines are involved in the molecular etiology of GIOP. Clinically, adults ≥40 years of age using glucocorticoids chronically with a high fracture risk are considered to have medical intervention. In addition to vitamin D and calcium tablet supplementations, the major therapeutic options approved for GIOP treatment include antiresorption drug bisphosphonates, parathyroid hormone N-terminal fragment teriparatide, and the monoclonal antibody denosumab. The selective estrogen receptor modulator can only be used under specific condition for postmenopausal women who have GIOP but fail to the regular GIOP treatment or have specific therapeutic contraindications. In this review, we focus on the molecular etiology of GIOP and the molecular pharmacology of the therapeutic drugs used for GIOP treatment.
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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.