Osteocyte Cellular Senescence
Open accessAbstract
Purpose of review Senescent cells are now known to accumulate in multiple tissues with aging and through their inflammation (the senescence-associated secretory phenotype, SASP) contribute to aging and chronic diseases. Here, we review the roles of senescent osteocytes in the context of bone loss.Recent findings Numerous studies have established that senescent osteocytes accumulate in the bone microenvironment with aging in mice and in humans. Moreover, at least in mice, elimination of senescent cells results in attenuation of age-related bone loss. Osteocyte senescence also occurs in response to other cellular stressors, including radiotherapy, chemotherapy, and metabolic dysfunction, where it appears to mediate skeletal deterioration. Osteocyte senescence is linked to bone loss associated with aging and other conditions. Senescent osteocytes are potential therapeutic targets to alleviate skeletal dysfunction. Additional studies better defining the underlying mechanisms as well as translating these exciting findings from mouse models to humans are needed.
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During aging, as well as under the action of several stressors, senescent osteocytes accumulate in the bone microenvironment and acquire a distinctive proinflammatory secretome, termed the senescence-associated secretory phenotype (SASP), which leads to imbalanced bone remodeling with increased resorption and decreased formation.
“In fact, during aging, as well as under the action of several stressors [see Farr et al.91 for a review], senescent osteocytes accumulate in the bone microenvironment and acquire a distinctive proinflammatory secretome, termed the senescence-associated secretory phenotype (SASP),92 which leads to imbalanced bone remodeling with increased resorption and decreased formation.”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [91]
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- Authors
- Farr, J. N., Kaur, J., Doolittle, M. L., & Khosla, S.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Farr, Joshua N.
- Venue
- Current Osteoporosis Reports
- Published
- 2020-08-13
- Volume
- 18
- Issue
- 5
- Pages
- 559-567
- ISSN
- 1544-1873 (ISSN-L)
- 1544-2241
- PMC
- PMC7541777
- OpenAlex
- W3049096591
- Cited by
- 60
- References
- 74
- Citations by year
- 2026: 17 · 2025: 13 · 2024: 14 · 2023: 9 · 2022: 4 · 2021: 2 · 2020: 1
- FWCI
- 0.51
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- Locations
- Current Osteoporosis Reports (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion, other-oa)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG062413, AG065868)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR070241)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- 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
- cellular senescence, senescence-associated secretory phenotype, bone loss, aging, senolytics, chemotherapy-induced bone loss, metabolic dysfunction, bone microenvironment
- MeSH terms
- Aging, Animals, Antineoplastic Agents, Diabetes Mellitus, Type 2, Humans, Osteocytes, Osteoporosis, Radiotherapy, Stress, Physiological, Cellular Senescence, Mice, Cellular Microenvironment
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