Klein Gordon L
Department of Orthopaedic Surgery and Rehabilitation, University of Texas Medical Branch, Galveston, TX 77555-0165, USA.
Int J Mol Sci. 2020 Dec 31;22(1):392. doi: 10.3390/ijms22010392.
This review describes the role of bone resorption in muscle atrophy as well as in muscle protein anabolism. Both catabolic and anabolic pathways involve components of the proinflammatory cytokine families and release of factors stored in bone during resorption. The juxtaposition of the catabolic and anabolic resorption-dependent pathways raises new questions about control of release of factors from bone, quantity of release in a variety of conditions, and relation of factors released from bone. The catabolic responses involve release of calcium from bone into the circulation resulting in increased inflammatory response in intensity and/or duration. The release of transforming growth factor beta (TGF-β) from bone suppresses phosphorylation of the AKT/mTOR pathway and stimulates ubiquitin-mediated breakdown of muscle protein. In contrast, muscle IL-6 production is stimulated by undercarboxylated osteocalcin, which signals osteoblasts to produce more RANK ligand, stimulating resorptive release of undercarboxylated osteocalcin, which in turn stimulates muscle fiber nutrient uptake and an increase in muscle mass.
本综述描述了骨吸收在肌肉萎缩以及肌肉蛋白合成代谢中的作用。分解代谢和合成代谢途径均涉及促炎细胞因子家族的成分以及骨吸收过程中储存于骨内的因子的释放。分解代谢和合成代谢性骨吸收依赖性途径的并列引发了关于骨内因子释放的控制、各种条件下的释放量以及骨释放因子之间关系的新问题。分解代谢反应包括骨中钙释放进入循环，导致炎症反应在强度和/或持续时间上增加。骨中转化生长因子β（TGF-β）的释放抑制AKT/mTOR途径的磷酸化，并刺激泛素介导的肌肉蛋白分解。相反，未羧化骨钙素刺激肌肉产生白细胞介素-6，其向成骨细胞发出信号以产生更多的核因子κB受体活化因子配体（RANKL），刺激未羧化骨钙素的吸收性释放，进而刺激肌纤维对营养物质的摄取并增加肌肉质量。
