[1] Klein-Nulend J, et al. Bone cell mechanosensitivity, estrogen deficiency, and osteoporosis. J Biomech.2015;48(5): 855-865.
[2] Jun ma, et al. Sodium hydrosulfide mitigates dexamethasone-induced osteoblast dysfunction by interfering with mitochondrial function. Biotechnol Appl Biochem.2019; 66(4):690-697.
[3] Hemmatian H, et al. Aging, Osteocytes, and Mechanotransduction. Curr Osteoporos Rep.2017; 15(5): 401-411.
[4] Rodan GA, Martin TJ. Therapeutic approaches to bone diseases. Science.2000; 289:1508-1514.
[5] Teitelbaum SL. Bone resorption by 0steoclasts. Science.2000; 289 :1504-1508.
[6] Ikebuchi, Y. et al. Coupling of bone resorption and formation by RANKL reverse signalling. Nature,2018; 561, 195–200.
[7] Kong YY, et al. Opgl is a key regulator of osteoclastogenesis lymphocyte development and lymph-node organogenesisi. Nature.1999; 397: 315-323.
[8] Karsenty G. Convergence between bone and energy homeostases: Leptin regulation of bone mass. Cell Metab.2006; 4: 341-348.
[9] Jeong E, et al. STAC2 negatively regulates osteoclast formation by targeting the RANK signaling complex. Cell Death Differ.2018; 25:1364–1374.
[10] Masuyama R, et al. Trpv4-mediated calcium influx regulates terminal differentiation of osteoclasts. Cell Metab.2008; 8:257-265.
[11] Hasegawa H, et al. Serum calcium-decreasing factor, caldecrin, inhibits osteoclast differentiation by suppression of nfatc1 activity. J Biol Chem.2010; 285:25448-25457.
[12] Kim MS, et al. Rankl-mediated reactive oxygen species pathway that induces long lasting ca2+ oscillations essential for osteoclastogenesis. J Biol Chem.2010; 285:6913-6921.
[13] Weber K, et al. Gene structure and regulation of the murine epithelial calcium channels ECaC1 and 2. Biochem Biophys Res Commun.2001; 289(5): 1287-1294.
[14] Schoeber JP, Hoenderop JG, Bindels RJ. Concerted action of associated proteins in the regulation of TRPV5 and TRPV6. Biochem-Soc-Trans.2007;35(1):115-119.
[15] Tengfei Song, et al. Regulation of TRPV5 transcription and expression by E2/ERa signalling contributes to inhibition of osteoclastogenesis. J Cell Mol Med.2018; 22(10):4738-4750.
[16] Chen F, et al. Knockout of TRPV6 causes osteopenia in mice by increasing osteoclastic differentiation and activity. Cell Physiol Biochem.2014; 33(3): 796-809.
[17] Bary EL. Expression of mRNA for the alpha 1 subunit of voltage-gated calcium channels in human osteoblast-like cell lines and normal human osteoblasts. Calcif Tissue Int.2000; 66(2): 145-150.
[18] Haussler MR, et al. Molecualr mechanisms of vitamin D action.2013; Calcif Tissue Int,92(2).
[19] Barthel TK, et al. 1,25-Dihydroxyvitamin D3/VDR-mediated induction of FGF23 as well as transcriptional control of other bone anabolic and catabolic genes that orchestrate the regulation of phosphate and calcium mineral metabolism. J Steroid Biochem Mol Biol.2007;103(3-5): 381-388.
[20] Bikle DD, et al. Role of IGF-I signaling in muscle bone interactions. Bone.2015; 80: 79-88.
[21] Yan J, et al.Gut microbiota induce IGF-1 and promote bone formation and growth. Proc Natl Acad Sci USA.2016;113(47).
[22] Duan C, Xu Q. Roles of insulin-like growth factor (IGF) binding proteins in regulating IGF actions. Gen Comp Endocrinol.2005;142(1-2): 44-52.
[23] Wang Y, et al. Role of IGF-I signaling in regulating osteoclastogenesis. J Bone Miner Res.2006;21(9):1350-1358.
[24] Bikle DD, Wang Y. Insulin like growth factor-I: a critical mediator of the skeletal response to parathyroid hormone. Curr Mol Pharmacol. 2012;5(2): 135-142.
[25] Xian L, et al. Matrix IGF-1 maintains bone mass by activation of mTOR in mesenchymal stem cells. Nat Med.2012; 18(7):1095-1101.
[26] Wang X, et al. A Liver-Bone Endocrine Relay by IGFBP1 Promotes Osteoclastogenesis and Mediates FGF21-Induced Bone Resorption. Cell Metab.2015;22(5): 811-24.
[27] DeMambro VE, et al. Insulin-like growth factor-binding protein-2 is required for osteoclast differentiation. J Bone Miner Res.2012;27(2): 390-400.
[28] Katsimbri P. The biology of normal bone remodelling. Eur J Can Care.2017;26:e12740.
[29] Ma J, et al. Hydrogen sulfide is a novel regulator implicated in glucocorticoids-inhibited bone formation. Aging-us.2019;11(18):7537-7552.
[30] Jun Ma, et al. Resveratrol Attenuates Lipopolysaccharides (LPS)-Induced Inhibition of Osteoblast Differentiation in MC3T3-E1 Cells. Med Sci Monit.2018;24:2045-2052.
[31] Jun Ma,et al. Metformin promotes differentiation of Human Bone Marrow Derived Mesenchymal Stem Cells into osteoblast via GSK3β inhibition. EUR REV MED PHARMACO.2018;22(22): 7962-7968.
[32] Bianco SD, et al. Marked disturbance of calcium homeostasis in mice with targeted disruption of the Trpv6 calcium channel gene. J Bone Miner Res.2007;22(2): 274-285.
[33] Lieben L, et al. Trpv6 mediates intestinal calcium absorption during calcium restriction and contributes to bone homeostasis. Bone.2010; 47(2): 301-308.
[34] Boyle WJ, Simonet WS, Lacey DL. Osteoclast differentiation and activation. Nature.2003;423(6937):337-342.
[35] Robling AG, Castillo AB, Turner CH. Biomechanical and molecular regulation of bone remodeling. Annu Rev Biomed Eng.2006;8(1):455-489.
[36] Hoenderop JG, et al. Function and expression of the epithelial Ca(2+) channel family: comparison of mammalian ECaC1 and 2. J Physiol.2001;537:747–761.
[37] Lapierre DM, et al. Lysophosphatidic acid signals through multiple receptors in osteoclasts to elevate cytosolic calcium concentration, evoke retraction, and promote cell survival. J Biol Chem.2010; 285(33): 25792-25801.
[38] Chang EJ, et al. The jnk-dependent camk pathway restrains the reversion of committed cells during osteoclast differentiation. J Cell Sci.2008;121:2555-2564.
[39] van der Eerden BC, Weissgerber P, Fratzl-Zelman N. The transient receptor potential channel trpv6 is dynamically expressed in bone cells but is not crucial for bone mineralization in mice. J Cell Physiol.2012;227:1951-1959.
[40] Zhou X, et al. Three-Dimensional Printed Titanium Scaffolds Enhance Osteogenic Differentiation and New Bone Formation by Cultured Adipose Tissue-Derived Stem Cells Through the IGF-1R/AKT/Mammalian Target of Rapamycin Complex 1 (mTORC1) Pathway. Med Sci Monit.2019;27;25:8043-8054.
[41] Tagliaferri C, et al. Muscle and bone, two interconnected tissues. Ageing Res Rev.2015;21:55-70.
[42] Dai W, et al. Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation. Cell Death Differ.2014;21(4): 568-81.
[43] Chen LL, et al. PI3K/AKT pathway involvement in the osteogenic effects of osteoclast culture supernatants on preosteoblast cells. Tissue Eng Part A.2013;19(19-20):2226-2632.
[44] Lee SE, et al. The phosphatidylinositol 3-kinase, p38, and extracellular signal-regulated kinase pathways are involved in osteoclast differentiation. Bone.2002;30:71–77.
[45] Xing R, et al. Interleukin-21 promotes osteoclastogenesis in RAW264.7 cells through the PI3 K/AKT signaling pathway independently of RANKL. Int J Mol Med.2016;38(4):1125–1134.