Cited by 101

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Targeting WNT signaling in the treatment of osteoporosis

Baron, Roland, Gori, Francesca·2018·Current Opinion in Pharmacology

Abstract

Osteoporosis is a widespread chronic disease characterized by low bone density, altered microstructure and bone fragility, leading to low impact fractures in affected individuals. The discovery of a few mutations that cause extremely rare human diseases has identified the WNT signaling pathway as a candidate for therapeutic intervention aimed at increasing bone mass and strength. In particular, inhibition of sclerostin, a WNT antagonist secreted by osteocytes, has proven in clinical trials to be a very efficient osteo-anabolic approach. One year of monthly administration of antibodies to sclerostin rapidly decreases bone resorption and increases bone formation and bone density at all sites, decreasing markedly fracture risk in treated patients. Their effect is however limited in time and cardiovascular adverse events have been reported in one clinical trial.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.coph.2018.04.011

Cites

9 of 9 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 9 references

Research works printed but not linked: 66

  1. Baron, 2011, Denosumab and bisphosphonates: different mechanisms of action and effects, Bone, 48, 677, 10.1016/j.bone.2010.11.020 · DOI
  2. Baron, 2012, Update on bone anabolics in osteoporosis treatment: rationale, current status, and perspectives, J Clin Endocrinol Metab, 97, 311, 10.1210/jc.2011-2332 · DOI
  3. Lindsay, 2007, Effects of a one-month treatment with PTH(1-34) on bone formation on cancellous, endocortical, and periosteal surfaces of the human ilium, J Bone Miner Res, 22, 495, 10.1359/jbmr.070104 · DOI
  4. Silva, 2015, Parathyroid hormone: anabolic and catabolic actions on the skeleton, Curr Opin Pharmacol, 22, 41, 10.1016/j.coph.2015.03.005 · DOI
  5. Gong, 2001, LDL receptor-related protein 5 (LRP5) affects bone accrual and eye development, Cell, 107, 513, 10.1016/S0092-8674(01)00571-2 · DOI · Paper page
  6. Little, 2002, A mutation in the LDL receptor-related protein 5 gene results in the autosomal dominant high-bone-mass trait, Am J Hum Genet, 70, 11, 10.1086/338450 · DOI · Paper page
  7. van Bezooijen, 2004, Sclerostin is an osteocyte-expressed negative regulator of bone formation, but not a classical BMP antagonist, J Exp Med, 199, 805, 10.1084/jem.20031454 · DOI
  8. Loots, 2005, Genomic deletion of a long-range bone enhancer misregulates sclerostin in Van Buchem disease, Genome Res, 15, 928, 10.1101/gr.3437105 · DOI · Paper page
  9. Balemans, 2002, Identification of a 52kb deletion downstream of the SOST gene in patients with van Buchem disease, J Med Genet, 39, 91, 10.1136/jmg.39.2.91 · DOI · Paper page
  10. Brunkow, 2001, Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein, Am J Hum Genet, 68, 577, 10.1086/318811 · DOI · Paper page
  11. Boudin, 2017, The Lrp4R1170Q homozygous knock-in mouse recapitulates the bone phenotype of sclerosteosis in humans, J Bone Miner Res, 32, 1739, 10.1002/jbmr.3160 · DOI
  12. Chang, 2014, Disruption of Lrp4 function by genetic deletion or pharmacological blockade increases bone mass and serum sclerostin levels, Proc Natl Acad Sci U S A, 111, E5187, 10.1073/pnas.1413828111 · DOI
  13. Fijalkowski, 2016, A novel domain-specific mutation in a sclerosteosis patient suggests a role of LRP4 as an anchor for sclerostin in human bone, J Bone Miner Res, 31, 874, 10.1002/jbmr.2782 · DOI
  14. Leupin, 2011, Bone overgrowth-associated mutations in the LRP4 gene impair sclerostin facilitator function, J Biol Chem, 286, 19489, 10.1074/jbc.M110.190330 · DOI
  15. Ellies, 2006, Bone density ligand, Sclerostin, directly interacts with LRP5 but not LRP5G171V to modulate Wnt activity, J Bone Miner Res, 21, 1738, 10.1359/jbmr.060810 · DOI
  16. Morvan, 2006, Deletion of a single allele of the Dkk1 gene leads to an increase in bone formation and bone mass, J Bone Miner Res, 21, 934, 10.1359/jbmr.060311 · DOI
  17. Richards, 2008, Bone mineral density, osteoporosis, and osteoporotic fractures: a genome-wide association study, Lancet, 371, 1505, 10.1016/S0140-6736(08)60599-1 · DOI
  18. Estrada, 2012, Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture, Nat Genet, 44, 491, 10.1038/ng.2249 · DOI
  19. Garcia-Ibarbia, 2013, Missense polymorphisms of the WNT16 gene are associated with bone mass, hip geometry and fractures, Osteoporos Int, 24, 2449, 10.1007/s00198-013-2302-0 · DOI
  20. Baron, 2013, WNT signaling in bone homeostasis and disease: from human mutations to treatments, Nat Med, 19, 179, 10.1038/nm.3074 · DOI · Paper page
  21. Brommage, 2015, Genetic approaches to identifying novel osteoporosis drug targets, J Cell Biochem, 116, 2139, 10.1002/jcb.25179 · DOI
  22. Kakugawa, 2015, Notum deacylates Wnt proteins to suppress signalling activity, Nature, 519, 187, 10.1038/nature14259 · DOI
  23. Glass, 2005, Canonical Wnt signaling in differentiated osteoblasts controls osteoclast differentiation, Dev Cell, 8, 751, 10.1016/j.devcel.2005.02.017 · DOI · Paper page
  24. Kramer, 2010, Osteocyte Wnt/beta-catenin signaling is required for normal bone homeostasis, Mol Cell Biol, 30, 3071, 10.1128/MCB.01428-09 · DOI
  25. Holmen, 2005, Essential role of beta-catenin in postnatal bone acquisition, J Biol Chem, 280, 21162, 10.1074/jbc.M501900200 · DOI · Paper page
  26. Wei, 2011, Biphasic and dosage-dependent regulation of osteoclastogenesis by beta-catenin, Mol Cell Biol, 31, 4706, 10.1128/MCB.05980-11 · DOI
  27. MacDonald, 2009, Wnt/beta-catenin signaling: components, mechanisms, and diseases, Dev Cell, 17, 9, 10.1016/j.devcel.2009.06.016 · DOI · Paper page
  28. Krishnamurthy, 2018, Targeting the Wnt/beta-catenin pathway in cancer: update on effectors and inhibitors, Cancer Treat Rev, 62, 50, 10.1016/j.ctrv.2017.11.002 · DOI
  29. Lin, 2014, Wnt signaling in osteosarcoma, Adv Exp Med Biol, 804, 33, 10.1007/978-3-319-04843-7_2 · DOI
  30. Prideaux, 2016, Osteocytes: the master cells in bone remodelling, Curr Opin Pharmacol, 28, 24, 10.1016/j.coph.2016.02.003 · DOI
  31. Gardner, 2005, Bone mineral density in sclerosteosis; affected individuals and gene carriers, J Clin Endocrinol Metab, 90, 6392, 10.1210/jc.2005-1235 · DOI
  32. Winkler, 2003, Osteocyte control of bone formation via sclerostin, a novel BMP antagonist, EMBO J, 22, 6267, 10.1093/emboj/cdg599 · DOI
  33. ten Dijke, 2008, Osteocyte-derived sclerostin inhibits bone formation: its role in bone morphogenetic protein and Wnt signaling, J Bone Joint Surg Am, 90, 31, 10.2106/JBJS.G.01183 · DOI
  34. Nakashima, 2011, Evidence for osteocyte regulation of bone homeostasis through RANKL expression, Nat Med, 17, 1231, 10.1038/nm.2452 · DOI · Paper page
  35. Xiong, 2011, Matrix-embedded cells control osteoclast formation, Nat Med, 17, 1235, 10.1038/nm.2448 · DOI · Paper page
  36. Li, 2009, Sclerostin antibody treatment increases bone formation, bone mass, and bone strength in a rat model of postmenopausal osteoporosis, J Bone Miner Res, 24, 578, 10.1359/jbmr.081206 · DOI
  37. Tian, 2011, Sclerostin antibody increases bone mass by stimulating bone formation and inhibiting bone resorption in a hindlimb-immobilization rat model, Bone, 48, 197, 10.1016/j.bone.2010.09.009 · DOI
  38. Li, 2008, Targeted deletion of the sclerostin gene in mice results in increased bone formation and bone strength, J Bone Miner Res, 23, 860, 10.1359/jbmr.080216 · DOI
  39. Li, 2010, Inhibition of sclerostin by monoclonal antibody increases bone formation, bone mass, and bone strength in aged male rats, J Bone Miner Res, 25, 2647, 10.1002/jbmr.182 · DOI
  40. Jacobsen, 2017, Application of anti-Sclerostin therapy in non-osteoporosis disease models, Bone, 96, 18, 10.1016/j.bone.2016.10.018 · DOI
  41. Ominsky, 2010, Two doses of sclerostin antibody in cynomolgus monkeys increases bone formation, bone mineral density, and bone strength, J Bone Miner Res, 25, 948, 10.1002/jbmr.14 · DOI
  42. Ominsky, 2014, Tissue-level mechanisms responsible for the increase in bone formation and bone volume by sclerostin antibody, J Bone Miner Res, 29, 1424, 10.1002/jbmr.2152 · DOI · Paper page
  43. Ominsky, 2017, Romosozumab improves bone mass and strength while maintaining bone quality in ovariectomized cynomolgus monkeys, J Bone Miner Res, 32, 788, 10.1002/jbmr.3036 · DOI
  44. Kim, 2017, Sclerostin antibody administration converts bone lining cells into active osteoblasts, J Bone Miner Res, 32, 892, 10.1002/jbmr.3038 · DOI
  45. Taylor, 2016, Time-dependent cellular and transcriptional changes in the osteoblast lineage associated with sclerostin antibody treatment in ovariectomized rats, Bone, 84, 148, 10.1016/j.bone.2015.12.013 · DOI · Paper page
  46. Ominsky, 2015, Differential temporal effects of sclerostin antibody and parathyroid hormone on cancellous and cortical bone and quantitative differences in effects on the osteoblast lineage in young intact rats, Bone, 81, 380, 10.1016/j.bone.2015.08.007 · DOI · Paper page
  47. Balani, 2017, Parathyroid hormone regulates fates of murine osteoblast precursors in vivo, J Clin Invest, 127, 3327, 10.1172/JCI91699 · DOI
  48. Jang, 2016, Intermittent PTH treatment can delay the transformation of mature osteoblasts into lining cells on the periosteal surfaces, J Bone Miner Metab, 34, 532, 10.1007/s00774-015-0707-x · DOI
  49. Suzuki, 2008, PTH/cAMP/PKA signaling facilitates canonical Wnt signaling via inactivation of glycogen synthase kinase-3beta in osteoblastic Saos-2 cells, J Cell Biochem, 104, 304, 10.1002/jcb.21626 · DOI
  50. Romero, 2010, Parathyroid hormone receptor directly interacts with dishevelled to regulate beta-Catenin signaling and osteoclastogenesis, J Biol Chem, 285, 14756, 10.1074/jbc.M110.102970 · DOI
  51. Tobimatsu, 2006, Parathyroid hormone increases beta-catenin levels through Smad3 in mouse osteoblastic cells, Endocrinology, 147, 2583, 10.1210/en.2005-1627 · DOI
  52. Wan, 2008, Parathyroid hormone signaling through low-density lipoprotein-related protein 6, Genes Dev, 22, 2968, 10.1101/gad.1702708 · DOI
  53. O’Brien, 2008, Control of bone mass and remodeling by PTH receptor signaling in osteocytes, PLoS ONE, 3, e2942, 10.1371/journal.pone.0002942 · DOI
  54. Kramer, 2012, Mef2c deletion in osteocytes results in increased bone mass, J Bone Miner Res, 27, 360, 10.1002/jbmr.1492 · DOI
  55. Guo, 2010, Suppression of Wnt signaling by Dkk1 attenuates PTH-mediated stromal cell response and new bone formation, Cell Metab, 11, 161, 10.1016/j.cmet.2009.12.007 · DOI
  56. Wein, 2016, SIKs control osteocyte responses to parathyroid hormone, Nat Commun, 7, 13176, 10.1038/ncomms13176 · DOI
  57. Wein, 2018, Regulation of bone remodeling by parathyroid hormone, Cold Spring Harb Perspect Med, 10.1101/cshperspect.a031237 · DOI
  58. Padhi, 2011, Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody, J Bone Miner Res, 26, 19, 10.1002/jbmr.173 · DOI
  59. McColm, 2014, Single- and multiple-dose randomized studies of blosozumab, a monoclonal antibody against sclerostin, in healthy postmenopausal women, J Bone Miner Res, 29, 935, 10.1002/jbmr.2092 · DOI
  60. Recker, 2015, A randomized, double-blind phase 2 clinical trial of blosozumab, a sclerostin antibody, in postmenopausal women with low bone mineral density, J Bone Miner Res, 30, 216, 10.1002/jbmr.2351 · DOI
  61. van Lierop, 2011, Patients with sclerosteosis and disease carriers: human models of the effect of sclerostin on bone turnover, J Bone Miner Res, 26, 2804, 10.1002/jbmr.474 · DOI
  62. van Lierop, 2014, Serum Dickkopf 1 levels in sclerostin deficiency, J Clin Endocrinol Metab, 99, E252, 10.1210/jc.2013-3278 · DOI
  63. Evenepoel, 2014, Romosozumab in postmenopausal women with osteopenia, N Engl J Med, 370, 1664, 10.1056/NEJMc1402396 · DOI
  64. Bostrom, 2011, The regulation of valvular and vascular sclerosis by osteogenic morphogens, Circ Res, 109, 564, 10.1161/CIRCRESAHA.110.234278 · DOI
  65. Hampson, 2013, The relationship between inhibitors of the Wnt signalling pathway (Dickkopf-1(DKK1) and sclerostin), bone mineral density, vascular calcification and arterial stiffness in post-menopausal women, Bone, 56, 42, 10.1016/j.bone.2013.05.010 · DOI
  66. van Lierop, 2013, Van Buchem disease: clinical, biochemical, and densitometric features of patients and disease carriers, J Bone Miner Res, 28, 848, 10.1002/jbmr.1794 · DOI

Cited by

Sorted by citations

See all 101

Metadata

Authors
Baron, R., & Gori, F.
Venue
Current Opinion in Pharmacology
Publisher
Elsevier BV
Published
2018-06
Volume
40
Pages
134-141
ISSN
1471-4892
Cited by
101
References
9
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review