Affordable Access

deepdyve-link
Publisher Website

Bone Aging, Cellular Senescence, and Osteoporosis

Authors
  • Pignolo, Robert J1, 1
  • Law, Susan F1
  • Chandra, Abhishek1, 1
  • 1 Mayo Clinic, USA , (United States)
Type
Published Article
Journal
JBMR Plus
Publisher
John Wiley & Sons, Inc.
Publication Date
Apr 02, 2021
Volume
5
Issue
4
Identifiers
DOI: 10.1002/jbm4.10488
PMID: 33869998
PMCID: PMC8046105
Source
PubMed Central
Keywords
Disciplines
  • Review
License
Unknown
External links

Abstract

Changes in aging bone that lead to osteoporosis are mediated at multiple levels, including hormonal alterations, skeletal unloading, and accumulation of senescent cells. This pathological interplay is superimposed upon medical conditions, potentially bone‐wasting medications, modifiable and unmodifiable personal risk factors, and genetic predisposition that accelerate bone loss with aging. In this study, the focus is on bone hemostasis and its dysregulation with aging. The major physiological changes with aging in bone and the role of cellular senescence in contributing to age‐related osteoporosis are summarized. The aspects of bone aging are reviewed including remodeling deficits, uncoupling phenomena, inducers of cellular senescence related to bone aging, roles of the senescence‐associated secretory phenotype, radiation‐induced bone loss as a model for bone aging, and the accumulation of senescent cells in the bone microenvironment as a predominant mechanism for age‐related osteoporosis. The study also addresses the rationale and potential for therapeutic interventions based on the clearance of senescent cells or suppression of the senescence‐associated secretory phenotype. © 2021 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

Report this publication

Statistics

Seen <100 times