Abstract
The decrease in bone mass and strength during aging has multiple causes. Osteocytes are long-lived cells within the bone matrix that perform a variety of functions, including the control of bone remodeling. Because of their longevity, osteocytes are more likely than osteoclasts or osteoblasts to accumulate molecular damage over time. Osteocytes utilize quality-control pathways like autophagy to remove damaged organelles and macromolecules, and thereby maintain function. When the damage is excessive, cell death pathways such as apoptosis minimize the impact of potential osteocyte dysfunction on the skeleton. The goal of this review is to discuss how dysregulation of these pathways in osteocytes may contribute to the decline in bone mass and strength with age.
Published Version
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