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Glucocorticoid induced autophagy in osteocytes
Open accessAbstract
Glucocorticoid (GC) therapy is the most frequent cause of secondary osteoporosis. In this study we have demonstrated that GC treatment induced the development of autophagy, preserving osteocyte viability. GC treatment resulted in an increase in autophagy markers and the accumulation of autophagosome vacuoles in vitro and in vivo promoted the onset of the osteocyte autophagy, as determined by expression of autophagy markers in an animal model of GC-induced osteoporosis. An autophagy inhibitor reversed the protective effects of GCs. The effects of GCs on osteocytes were in contrast to tumor necrosis factor α (TNF-α), which induced apoptosis but not autophagy. Together this study reveals a novel mechanism for the effect of GC on osteocytes, shedding new insight into mechanisms responsible for bone loss in patients receiving GC therapy.
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“We have reported that osteocyte autophagy is crucial to the regulation of bone structure and plays a role in GC induced bone fragility [44, 68].”
From Prevention of glucocorticoid induced bone changes with beta-ecdysone (2015) · cites this paper as [68]
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Bonewald, L. F. (2011) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.320 · Cited by 2,287
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Background
Metadata
- Authors
- Xia, X., Kar, R., Gluhak-Heinrich, J., Yao, W., Lane, N. E., Bonewald, L. F., Biswas, S. K., Lo, W.-K., & Jiang, J. X.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Department of Orthodontics, University of Texas Health Science Center, San Antonio, TX, USA
- University of California Davis Medical Center (US)
- University of Missouri–Kansas City (US)
- Morehouse School of Medicine (US)
- Corresponding author
- Jiang, Jean X
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-10-25
- Volume
- 25
- Issue
- 11
- Pages
- 2479-2488
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- PMC
- PMC3179284
- OpenAlex
- W2004485238
- Cited by
- 193
- References
- 33
- Citations by year
- 2026: 8 · 2025: 3 · 2024: 4 · 2023: 9 · 2022: 8 · 2021: 12 · 2020: 12 · 2019: 13 · 2018: 16 · 2017: 11 · 2016: 12 · 2015: 18 · 2014: 22 · 2013: 21 · 2012: 16
- FWCI
- 10.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Journal of Bone and Mineral Research (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Tokyo Medical and Dental University
- National Institutes of Health (AQ‐1507, and K24, AR46798)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (K24-AR04884, R01AR043052, K24AR048841, P01AR046798, P01AR46798)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12 HD05195801, K12HD051958)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- glucocorticoids, autophagy, osteocytes, glucocorticoid-induced osteoporosis, autophagosomes, osteocyte viability, autophagy inhibition, TNF-α, apoptosis, bone loss
- MeSH terms
- Adenine, Animals, Autophagy, Cell Count, Cell Line, Chickens, Dexamethasone, Glucocorticoids, Microtubule-Associated Proteins, Osteocytes, Phagosomes, Biomarkers, Apoptosis, Rats
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