[1]Salazar VS, Gamer LW, Rosen V.BMP signalling in skeletal development, disease and repair[J].Nat Rev Endocrinol, 2016, 12(4):203-221[2]Garg P, Mazur MM, Buck AC, et al.Prospective Review of Mesenchymal Stem Cells Differentiation into Osteoblasts[J].Orthop Surg, 2017, 9(1):13-19[3]Chen G, Deng C, Li YP.TGF-β and BMP signaling in osteoblast differentiation and bone formation[J].Int J Biol Sci, 2012, 8(2):272-288[4]Kamiya N, Kaartinen VM, Mishina Y.Loss-of-function of ACVR1 in osteoblasts increases bone mass and activates canonical Wnt signaling through suppression of Wnt inhibitors SOST and DKK1[J].Biochem Biophys Res Commun, 2011, 414(2):326-330[5]Long F.Building strong bones: molecular regulation of the osteoblast lineage[J].Nat Rev Mol Cell Biol, 2011, 13(1):27-38[6]Karmali PP, Chaudhuri A.Cationic liposomes as non-viral carriers of gene medicines: resolved issues, open questions, and future promises[J].Med Res Rev, 2007, 27(5):696-722[7]Dudas M, Sridurongrit S, Nagy A, et al.Craniofacial defects in mice lacking BMP type I receptor Alk2 in neural crest cells[J].Mech Dev, 2004, 121(2):173-182[8]Agarwal S, Loder SJ, Brownley C, et al.BMP signaling mediated by constitutively active Activin type 1 receptor (ACVR1) results in ectopic bone formation localized to distal extremity joints[J].Dev Biol, 2015, 400(2):202-209 |