Yuhei Uda1, Ehab Azab1, Ningyuan Sun1, Chao Shi1,2, Paola Divieti Pajevic3,4. 1. Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, USA. 2. Department of Orthopaedics, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, Shaanxi Province, People's Republic of China. 3. Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, USA. pdivieti@bu.edu. 4. , 700 Albany Street, W201C, Boston, MA, 02118, USA. pdivieti@bu.edu.
Abstract
PURPOSE OF REVIEW: Over the past decades, osteocytes have emerged as mechano-sensors of bone and master regulators of bone homeostasis. This article summarizes latest research and progress made in understanding osteocyte mechanobiology and critically reviews tools currently available to study these cells. RECENT FINDINGS: Whereas increased mechanical forces promote bone formation, decrease loading is always associated with bone loss and skeletal fragility. Recent studies identified cilia, integrins, calcium channels, and G-protein coupled receptors as important sensors of mechanical forces and Ca2+ and cAMP signaling as key effectors. Among transcripts regulated by mechanical forces, sclerostin and RANKL have emerged as potential therapeutic targets for disuse-induced bone loss. In this paper, we review the mechanisms by which osteocytes perceive and transduce mechanical cues and the models available to study mechano-transduction. Future directions of the field are also discussed.
PURPOSE OF REVIEW: Over the past decades, osteocytes have emerged as mechano-sensors of bone and master regulators of bone homeostasis. This article summarizes latest research and progress made in understanding osteocyte mechanobiology and critically reviews tools currently available to study these cells. RECENT FINDINGS: Whereas increased mechanical forces promote bone formation, decrease loading is always associated with bone loss and skeletal fragility. Recent studies identified cilia, integrins, calcium channels, and G-protein coupled receptors as important sensors of mechanical forces and Ca2+ and cAMP signaling as key effectors. Among transcripts regulated by mechanical forces, sclerostin and RANKL have emerged as potential therapeutic targets for disuse-induced bone loss. In this paper, we review the mechanisms by which osteocytes perceive and transduce mechanical cues and the models available to study mechano-transduction. Future directions of the field are also discussed.
Entities:
Keywords:
Bone homeostasis; Mechanical forces; Osteocyte; Sclerostin
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