ArticleEndocrine connections2019
Regulation of sclerostin in glucocorticoid-induced osteoporosis (GIO) in mice and humans.
Article in Endocrine connections, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Romosozumab for the treatment of osteoporosis - a systematic review.Journal of endocrinological investigation · 2025Pooled it
- Evaluation of Mandibular Bone Alterations by Panoramic Radiography: A Potential Tool in the Identification of Signs of Osteopenia and Osteoporosis.Bioengineering (Basel, Switzerland) · 2025Article
- EndoCompass Project: Research Roadmap for Calcium and Bone Endocrinology.Hormone research in paediatrics · 2025Review
- Treatment of glucocorticoid-induced osteoporosis with concurrent denosumab and romosozumab: a case report.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024Article
- Association of serum sclerostin levels with marrow adiposity in postmenopausal women with glucocorticoid-induced osteoporosis.BMC endocrine disorders · 2024Article
- Bone Turnover Markers: Basic Biology to Clinical Applications.Endocrine reviews · 2023Article
- Partial prevention of glucocorticoid-induced osteocyte deterioration in young male mice with osteocrin gene therapy.iScience · 2022Article
- The Role of Sclerostin in Bone Diseases.Journal of clinical medicine · 2022Review
- Bad to the Bone: The Effects of Therapeutic Glucocorticoids on Osteoblasts and Osteocytes.Frontiers in endocrinology · 2022Review
- Effects of romosozumab or denosumab treatment on the bone mineral density and disease activity for 6 months in patients with rheumatoid arthritis with severe osteoporosis: An open-label, randomized, pilot study.Osteoporosis and sarcopenia · 2021Article
- Hesperetin alleviated glucocorticoid-induced inhibition of osteogenic differentiation of BMSCs through regulating the ERK signaling pathway.Medical molecular morphology · 2021Article
- Icariin Promotes the Osteogenesis of Bone Marrow Mesenchymal Stem Cells through Regulating Sclerostin and Activating the Wnt/BioMed research international · 2021Article
- Wnt Inhibitors and Bone Turnover Markers in Patients With Polymyalgia Rheumatica and Acute Effects of Glucocorticoid Treatment.Frontiers in medicine · 2020Article
- The molecular etiology and treatment of glucocorticoid-induced osteoporosis.Tzu chi medical journalReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Glucocorticoids (GC) are used for the treatment of inflammatory diseases, including various forms of arthritis. However, their use is limited, amongst others, by adverse effects on bone. The Wnt and bone formation inhibitor sclerostin was recently implicated in the pathogenesis of GC-induced osteoporosis. However, data are ambiguous. The aim of this study was to assess the regulation of sclerostin by GC using several mouse models with high GC levels and two independent cohorts of patients treated with GC. Male 24-week-old C57BL/6 and 18-week-old DBA/1 mice exposed to GC and 12-week-old mice with endogenous hypercortisolism displayed reduced bone formation as indicated by reduced levels of P1NP and increased serum sclerostin levels. The expression of sclerostin in femoral bone tissue and GC-treated bone marrow stromal cells, however, was not consistently altered. In contrast, GC dose- and time-dependently suppressed sclerostin at mRNA and protein levels in human mesenchymal stromal cells, and this effect was GC receptor dependent. In line with the human cell culture data, patients with rheumatoid arthritis (RA, n = 101) and polymyalgia rheumatica (PMR, n = 21) who were exposed to GC had lower serum levels of sclerostin than healthy age- and sex-matched controls (-40%, P < 0.01 and -26.5%, P < 0.001, respectively). In summary, sclerostin appears to be differentially regulated by GC in mice and humans as it is suppressed by GCs in humans but is not consistently altered in mice. Further studies are required to delineate the differences between GC regulation of sclerostin in mice and humans and assess whether sclerostin mediates GC-induced osteoporosis in humans.
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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.