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Cited by 201Bone health and osteoporosis researchBone Metabolism and DiseasesEstrogen and related hormone effects

The DOI matches its Crossref record; 80 of the 80 references it cites were found in a registry or an index.

Molecular mechanisms of glucocorticoid-induced osteoporosis.

Patschan, D., Loddenkemper, K., Buttgereit, F.·2001·Bone
DOI 10.1016/s8756-3282(01)00610-x
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Abstract

Bone loss resulting from long-term glucocorticoid therapy is common and clinically relevant. A number of different glucocorticoid-mediated effects are responsible for the reduction in bone density: (i) glucocorticoid-induced direct impairment of osteoblast, osteocyte, and osteoclast function leads to reduced bone remodeling and diminished repair of microdamage in bone; (ii) the effects of parathyroid hormone (PTH) might be more pronounced in the presence of glucocorticoids, whereas vitamin D plays a lesser role in the pathogenesis of steroid-induced osteoporosis; (iii) glucocorticoids antagonize gonadal function and inhibit the osteoanabolic action of sex steroids; and (iv) increased renal elimination and reduced intestinal absorption of calcium lead to a negative calcium balance that has been suggested to promote secondary hyperparathyroidism. From a mechanistic point of view, all of the aforementioned effects have long been considered to be mediated at the molecular level exclusively by genomic actions. However, there is now increasing evidence for the existence of rapid glucocorticoid effects that are incompatible with this classical mode of action. These rapid effects, termed nongenomic effects, are mediated by glucocorticoid interactions with biological membranes, either through binding to membrane receptors or by physicochemical interactions. It is possible, but has yet to be shown, that these effects play a role in the pathogenesis of glucocorticoid-induced osteoporosis.

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Crossref · 10.1016/s8756-3282(01)00610-x

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Research works printed but not linked: 3

  1. Chen, 1999, Multiple glucocorticoid receptor transcripts in membrane glucocorticoid receptor-enriched S-49 mouse lymphoma cells, J Cell Biochem, 74, 418, 10.1002/(SICI)1097-4644(19990901)74:3<418::AID-JCB10>3.0.CO;2-6 · DOI
  2. Conover, 1996, Insulin-like growth factor-binding protein-1 expression in cultured human bone cells, Endocrinology, 137, 3295, 10.1210/en.137.8.3295 · DOI
  3. Lian, 1997, Species-specific glucocorticoid and 1,25-dihydroxyvitamin D responsiveness in mouse. MC3T3-E1 osteoblasts, Endocrinology, 138, 2117, 10.1210/en.138.5.2117 · DOI · Paper page

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Metadata

Authors
Patschan, D., Loddenkemper, K., & Buttgereit, F.
Affiliations
Humboldt-Universität zu Berlin (DE)
Corresponding author
Buttgereit, F.
ORCID
Venue
Bone
Publisher
Elsevier BV
Published
2001-12
Volume
29
Issue
6
Pages
498-505
ISSN
  • 1873-2763 (ISSN-L)
  • 8756-3282
DOI
10.1016/s8756-3282(01)00610-x
OpenAlex
W2005326563
Cited by
201
References
80
Citations by year
2026: 2 · 2025: 7 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 11 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 6 · 2016: 8 · 2015: 9 · 2014: 8 · 2013: 6 · 2012: 6
FWCI
8.19
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Bone (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Keywords
glucocorticoid-induced osteoporosis, bone loss, bone remodeling, osteoblast activity, osteoclast function, osteocyte function, parathyroid hormone, vitamin D, sex steroids, gonadal function, calcium balance, secondary hyperparathyroidism, glucocorticoid receptor signaling
MeSH terms
Calcium, Glucocorticoids, Humans, Intestinal Absorption, Kidney, Osteoblasts, Osteoclasts, Osteoporosis, Parathyroid Hormone, Gonadal Steroid Hormones, Vitamin D

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