Cited by 20Bone Metabolism and DiseasesBone health and osteoporosis researchParathyroid Disorders and Treatments

Parathyroid hormone signaling in mature osteoblasts/osteocytes protects mice from age-related bone loss

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Uda, Yuhei, Saini, Vaibhav, Petty, Christopher A., Alshehri, Majed, Shi, Chao, Spatz, Jordan M., Santos, Roberto, Newell, Carly M. +8 more·2021·Aging

Abstract

studies demonstrated that PTH protects osteocytes from oxidative stress-induced cell death. In summary, we reported that PPR signaling in osteocytes is important for protecting the skeleton from age-induced bone loss by restraining osteoclast's activity and protecting osteocytes from oxidative stresses.

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Crossref · 10.18632/aging.203808

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  • When PTHR1 was deleted in mouse osteocytes in vivo (Dmp1-PPRKO), the affected mice displayed age-dependent osteopenia related to a decrease in osteoblast activity with a parallel rise in osteoclast number and activity; the imbalanced bone remodeling was partially due to a sclerostin-dependent decrease in osteoblast activity and the lack of osteocyte protection from oxidative stress.

    “When PTHR1 was deleted in mouse osteocytes in vivo (Dmp1-PPRKO), the affected mice displayed age-dependent osteopenia related to a decrease in osteoblast activity with a parallel rise in osteoclast number and activity. The imbalanced bone remodeling in these animals was partially due to a sclerostin-dependent decrease in osteoblast activity and the lack of osteocyte protection from oxidative”

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Authors
Uda, Y., Saini, V., Petty, C. A., Alshehri, M., Shi, C., Spatz, J. M., Santos, R., Newell, C. M., Huang, T. Y., Kochen, A., Kim, J. W., Constantinou, C. K., Saito, H., Held, K. D., Hesse, E., & Pajevic, P. D.
Affiliations
  • Boston University (US)
  • Harvard University (US)
  • University Medical Center Hamburg-Eppendorf (DE)
Corresponding author
Pajevic, Paola Divieti
Venue
Aging
Published
2021-12-30
Volume
13
Issue
24
Pages
25607-25642
ISSN
1945-4589 (ISSN-L)
OpenAlex
W4200071064
Cited by
20
References
55
Citations by year
2026: 1 · 2025: 7 · 2024: 6 · 2023: 4 · 2022: 2
FWCI
0.94
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Aging (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1s10od021652-01, DK079161)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R56DK079161, AR060221, R01DK079161)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR060221, P30AR066261, UH3AR059655, UH2AR059655)
Topics
  • 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
  • Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
Keywords
parathyroid hormone signaling, osteoblasts, osteocytes, age-related bone loss, osteoclast activity, oxidative stress, bone aging
MeSH terms
Animals, Bone and Bones, Bone Diseases, Metabolic, Bone Resorption, Homeostasis, Osteoblasts, Osteoclasts, Osteocytes, Osteoporosis, Parathyroid Hormone, Signal Transduction, Mice, Knockout, Receptor, Parathyroid Hormone, Type 1, Mice

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