Jilka Robert L, O'Brien Charles A
Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Curr Osteoporos Rep. 2016 Feb;14(1):16-25. doi: 10.1007/s11914-016-0297-0.
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.
衰老过程中骨量和骨强度的下降有多种原因。骨细胞是骨基质中的长寿细胞,执行多种功能,包括控制骨重塑。由于其长寿,随着时间的推移,骨细胞比破骨细胞或成骨细胞更有可能积累分子损伤。骨细胞利用自噬等质量控制途径清除受损的细胞器和大分子,从而维持功能。当损伤过度时,细胞凋亡等细胞死亡途径可将潜在的骨细胞功能障碍对骨骼的影响降至最低。本综述的目的是讨论骨细胞中这些途径的失调如何可能导致随着年龄增长骨量和骨强度的下降。