Deconstructing cellular senescence in bone and beyond

Research output: Contribution to journalResearch articleContributedpeer-review


Osteocytes are specialized bone cells that orchestrate skeletal remodeling. Senescent osteocytes are characterized by an activation of cyclin-dependent kinase inhibitor p16Ink4a and have been implicated in the pathogenesis of several bone loss disorders. In this issue of the JCI, Farr et al. have now shown that systemic removal of senescent cells (termed senolysis) prevented age-related bone loss at the spine and femur and mitigated bone marrow adiposity through a robust effect on osteoblasts and osteoclasts, whereas cell-specific senolysis in osteocytes alone was only partially effective. Surprisingly, transplantation of senescent fibroblasts into the peritoneum of young mice caused host osteocyte senescence associated with bone loss. This refined concept of osteocyte senescence and the effects of remote senolysis may help to develop improved senolytic strategies against multisystem aging in bone and beyond.


Original languageEnglish
Article numbere169069
Number of pages4
JournalJournal of Clinical Investigation
Issue number8
Publication statusPublished - 17 Apr 2023

External IDs

PubMed 37066877
unpaywall 10.1172/jci169069
Mendeley e6d79c5f-79c9-37c9-9454-ae0ff6f66721
WOS 000982479400003
ORCID /0000-0002-8691-8423/work/142236076


Research priority areas of TU Dresden

Subject groups, research areas, subject areas according to Destatis

Sustainable Development Goals

ASJC Scopus subject areas


  • Mice, Animals, Cellular Senescence/physiology, Bone and Bones, Aging/pathology, Osteoblasts, Osteoclasts, Osteocytes, Bone Diseases, Metabolic

Library keywords