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Targeting Cell Senescence for the Treatment of Age-Related Bone Loss

  • Therapeutics and Medical Management (S Jan de Beur and B Clarke, Section Editors)
  • Published:
Current Osteoporosis Reports Aims and scope Submit manuscript

Abstract

Purpose of Review

We review cell senescence in the context of age-related bone loss by broadly discussing aging mechanisms in bone, currently known inducers and markers of senescence, the senescence-associated secretory phenotype (SASP), and the emerging roles of senescence in bone homeostasis and pathology.

Recent Findings

Cellular senescence is a state of irreversible cell cycle arrest induced by insults or stressors including telomere attrition, oxidative stress, DNA damage, oncogene activation, and other intrinsic or extrinsic triggers and there is mounting evidence for the role of senescence in aging bone. Cellular aging also instigates a SASP that exerts detrimental paracrine and likely systemic effects.

Summary

With aging, multiple cell types in the bone microenvironment become senescent, with osteocytes and myeloid cells as primary contributors to the SASP. Targeting undesired senescent cells may be a favorable strategy to promote bone anabolic and anti-resorptive functions in aging bone, with the possibility of improving bone quality and function with normal aging and/or disease.

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Acknowledgements

This work was supported by the Robert and Arlene Kogod Professorship in Geriatric Medicine (to RJP) and a Robert and Arlene Kogod Center on Aging career development award (to RMS).

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Correspondence to Robert J. Pignolo.

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Robert Pignolo, Rebekah Samsonraj, Susan Law, Haitao Wang and Abhishek Chandra declare no conflict of interest.

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Pignolo, R.J., Samsonraj, R.M., Law, S.F. et al. Targeting Cell Senescence for the Treatment of Age-Related Bone Loss. Curr Osteoporos Rep 17, 70–85 (2019). https://doi.org/10.1007/s11914-019-00504-2

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