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Erschienen in: Current Osteoporosis Reports 3/2015

01.06.2015 | Kidney and Bone (SM Moe and IB Salusky, Section Editors)

Sclerostin and CKD-MBD

verfasst von: Susan C. Schiavi

Erschienen in: Current Osteoporosis Reports | Ausgabe 3/2015

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Abstract

Declining kidney function is associated with sequential systemic changes in mineral homeostasis leading to pathologic alterations in the cardiovascular system and the skeleton. One of the earliest changes in response to renal injury is the increased osteocyte production of secreted factors including the anti-anabolic protein, sclerostin. Elevated sclerostin is associated with reduced Wnt/β-catenin signaling in bone and decreased osteoblast differentiation/activity. Agents that directly or indirectly inhibit β-catenin signaling have differential skeletal effects suggesting additional mechanisms contribute to the diversity of renal osteodystrophies. Similarly, Wnt/β-catenin activation in smooth muscle cells contributes to cardiovascular calcification yet emerging data suggests that this pathway may also be protective when elevated in neighboring tissues. The ongoing epidemiology studies examining the relationship between circulating sclerostin and cardiovascular disease, particularly those that investigate stage specific and/or patient sub-populations, will be useful in understanding the overall contributions of this pathway, its antagonist sclerostin, and the progression of CKD-MBD.
Literatur
1.
Zurück zum Zitat Moe S, Drueke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from kidney disease: improving global outcomes (KDIGO). Kidney Int. 2006;69:1945–53.CrossRefPubMed Moe S, Drueke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from kidney disease: improving global outcomes (KDIGO). Kidney Int. 2006;69:1945–53.CrossRefPubMed
2.
Zurück zum Zitat Moe SM. Definition and classification of renal osteodystrophy and chronic kidney disease-mineral bone disorder (CKD-MBD). In: Olgaard K, Salusky IB, Silver J, editors. The spectrum of mineral and bone disorders in chronic kidney disease. New York: Oxford University; 2010. p. 1–14.CrossRef Moe SM. Definition and classification of renal osteodystrophy and chronic kidney disease-mineral bone disorder (CKD-MBD). In: Olgaard K, Salusky IB, Silver J, editors. The spectrum of mineral and bone disorders in chronic kidney disease. New York: Oxford University; 2010. p. 1–14.CrossRef
3.•
Zurück zum Zitat Lu K-C, Wu C-C, Yen JF. Vascular calcification and renal bone disorders. Sci World J. 2014;637065:1–20. A comprehensive review summarizing the link between poor bone health and cardiovascular disease in CKD. Lu K-C, Wu C-C, Yen JF. Vascular calcification and renal bone disorders. Sci World J. 2014;637065:1–20. A comprehensive review summarizing the link between poor bone health and cardiovascular disease in CKD.
4.
Zurück zum Zitat Cannata-Andia JB, Roan-Garcia P, Hruska K. The connections between vascular calcification and bone health. Nephrol Dial Transplant. 2011;26:3429–36.CrossRefPubMedCentralPubMed Cannata-Andia JB, Roan-Garcia P, Hruska K. The connections between vascular calcification and bone health. Nephrol Dial Transplant. 2011;26:3429–36.CrossRefPubMedCentralPubMed
5.
Zurück zum Zitat Hu MC, Shiizaki K, Kuro-o M, Moe OW. Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol. 2013;75:503–33.CrossRefPubMedCentralPubMed Hu MC, Shiizaki K, Kuro-o M, Moe OW. Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol. 2013;75:503–33.CrossRefPubMedCentralPubMed
6.
Zurück zum Zitat Quarles D. A systems biology preview of the relationships between mineral and metabolic complications in chronic kidney disease. Semin Nephrol. 2013;33:130–42.CrossRefPubMed Quarles D. A systems biology preview of the relationships between mineral and metabolic complications in chronic kidney disease. Semin Nephrol. 2013;33:130–42.CrossRefPubMed
7.
Zurück zum Zitat Krisnan V, Bryant HU, MacDougald OA. Regulation of bone mass by Wnt signaling. J Clin Invest. 2006;116:1202–9.CrossRef Krisnan V, Bryant HU, MacDougald OA. Regulation of bone mass by Wnt signaling. J Clin Invest. 2006;116:1202–9.CrossRef
8.••
Zurück zum Zitat Baron R, Kneissel M. WNT signaling in bone homeostasis and disease: from human mutations to treatments. Nature Med. 2013;19:179–92. Outstanding review article describing evidence based mechanistic understanding of canonical Wnt/β-catenin signaling and its role in bone biology.CrossRefPubMed Baron R, Kneissel M. WNT signaling in bone homeostasis and disease: from human mutations to treatments. Nature Med. 2013;19:179–92. Outstanding review article describing evidence based mechanistic understanding of canonical Wnt/β-catenin signaling and its role in bone biology.CrossRefPubMed
9.
Zurück zum Zitat Modder UI, Hoey KA, Amin S, et al. Relation of age, gender, and bone mass to circulating sclerostin levels in women and men. J Bone Miner Res. 2011;26:373–9.CrossRefPubMedCentralPubMed Modder UI, Hoey KA, Amin S, et al. Relation of age, gender, and bone mass to circulating sclerostin levels in women and men. J Bone Miner Res. 2011;26:373–9.CrossRefPubMedCentralPubMed
10.
Zurück zum Zitat Li X, Ominsky MS, Warminghton KS, et al. Sclerostin antibody treatment increases bone formation, bone mass, and bone strength in a rat model of post-menopausal osteoporosis. J Bone Miner Res. 2009;24:578–88.CrossRefPubMed Li X, Ominsky MS, Warminghton KS, et al. Sclerostin antibody treatment increases bone formation, bone mass, and bone strength in a rat model of post-menopausal osteoporosis. J Bone Miner Res. 2009;24:578–88.CrossRefPubMed
11.
Zurück zum Zitat Ominsky MS, Vlasseros F, Jolette J, et al. Two doses of anti-sclerostin antibody in cynomologus monkeys increases bone formation, bone mieral density, and bone strength. J Bone Miner Res. 2010;25:948–59.CrossRefPubMed Ominsky MS, Vlasseros F, Jolette J, et al. Two doses of anti-sclerostin antibody in cynomologus monkeys increases bone formation, bone mieral density, and bone strength. J Bone Miner Res. 2010;25:948–59.CrossRefPubMed
12.
Zurück zum Zitat Padhi D, Jang G, Stouch B, et al. Single dose placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. J Bone Miner Res. 2011;26:19–26.CrossRefPubMed Padhi D, Jang G, Stouch B, et al. Single dose placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. J Bone Miner Res. 2011;26:19–26.CrossRefPubMed
14.
Zurück zum Zitat Poole KE, Reeve J. Parathyroid hormone: a double-edged sword for bone metabolism. Curr Opin Pharmacol. 2005;5:612–7.CrossRefPubMed Poole KE, Reeve J. Parathyroid hormone: a double-edged sword for bone metabolism. Curr Opin Pharmacol. 2005;5:612–7.CrossRefPubMed
15.
Zurück zum Zitat Kramer I, Kellar H, Leupin O, Kniessel M. Does osteocytic SOST suppression mediate PTH anabolism? Trends in Endocr Metab. 2010;21:237–44.CrossRef Kramer I, Kellar H, Leupin O, Kniessel M. Does osteocytic SOST suppression mediate PTH anabolism? Trends in Endocr Metab. 2010;21:237–44.CrossRef
17.
Zurück zum Zitat Brandenburg VM, Floege J. Adynamic bone disease—bone and beyond. Nephrol Dial Transpl. 2008;3:135–47. Brandenburg VM, Floege J. Adynamic bone disease—bone and beyond. Nephrol Dial Transpl. 2008;3:135–47.
18.
Zurück zum Zitat Rocha LA, Higa A, Barreto FC, et al. Variant of adynamic bone disease in hemodialysis patients: fact or fiction? Am J Kidney Dis. 2006;48:430–6.CrossRefPubMed Rocha LA, Higa A, Barreto FC, et al. Variant of adynamic bone disease in hemodialysis patients: fact or fiction? Am J Kidney Dis. 2006;48:430–6.CrossRefPubMed
19.
Zurück zum Zitat Lund RJ, Davies MR, Matthew S, Hruska K. New discoveries in the pathogenesis of renal osteodystrophy. J Bone Miner Res. 2006;24:169–71.CrossRef Lund RJ, Davies MR, Matthew S, Hruska K. New discoveries in the pathogenesis of renal osteodystrophy. J Bone Miner Res. 2006;24:169–71.CrossRef
20.••
Zurück zum Zitat Sabbagh Y, Graciolli FG, O’Brien S, et al. Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy. J Bone Min Res. 2012;27:1757–72. First mechanistic evidence that repression of Wnt/β-catenin signaling is associated with CKD in mouse bones and clinical biopsies.CrossRef Sabbagh Y, Graciolli FG, O’Brien S, et al. Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy. J Bone Min Res. 2012;27:1757–72. First mechanistic evidence that repression of Wnt/β-catenin signaling is associated with CKD in mouse bones and clinical biopsies.CrossRef
21.
Zurück zum Zitat Kramer I, Halleux C, Keller H, et al. Osteocyte Wnt/beta-catenin signaling is required for normal bone homeostasis. Mol Cell Biol. 2010;30:3072–85.CrossRef Kramer I, Halleux C, Keller H, et al. Osteocyte Wnt/beta-catenin signaling is required for normal bone homeostasis. Mol Cell Biol. 2010;30:3072–85.CrossRef
22.
Zurück zum Zitat Wijenayaka AR, Kogawa M, Lim HP. Sclerostin stimulates osteocyte support of osteoclast activity by a RANKL-dependent pathway. PLoS One. 2011;10:e25900.CrossRef Wijenayaka AR, Kogawa M, Lim HP. Sclerostin stimulates osteocyte support of osteoclast activity by a RANKL-dependent pathway. PLoS One. 2011;10:e25900.CrossRef
23.
Zurück zum Zitat Moyses R. Osteocyte regulation in renal osteodystrophy. Presented Am Soc Nephrology, Philadelphia, PA, 2014. Moyses R. Osteocyte regulation in renal osteodystrophy. Presented Am Soc Nephrology, Philadelphia, PA, 2014.
24.
Zurück zum Zitat Bellido T, Ali AA, Gubrij I, et al. Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesis. Endocrinology. 2005;146:4577–83.CrossRefPubMed Bellido T, Ali AA, Gubrij I, et al. Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesis. Endocrinology. 2005;146:4577–83.CrossRefPubMed
25.
26.••
Zurück zum Zitat Moe SM, Chen NX, Newman CL, et al. Anti-sclerostin antibody treatment in a rat model of progressive renal osteodystrophy. J Bone Miner Res. 2014. doi:10.1002/jbmr.2372. Describes preclinical effects of anti-sclerostin antibody on low and not high bone turnover.PubMedCentral Moe SM, Chen NX, Newman CL, et al. Anti-sclerostin antibody treatment in a rat model of progressive renal osteodystrophy. J Bone Miner Res. 2014. doi:10.​1002/​jbmr.​2372. Describes preclinical effects of anti-sclerostin antibody on low and not high bone turnover.PubMedCentral
27.
Zurück zum Zitat Fang Y, Ginsberg C, Sugatani T, et al. Early chronic kidney disease-mineral bone disorder stimulates vascular calcification. Kidney Intern. 2013;85:142–50.CrossRef Fang Y, Ginsberg C, Sugatani T, et al. Early chronic kidney disease-mineral bone disorder stimulates vascular calcification. Kidney Intern. 2013;85:142–50.CrossRef
28.•
Zurück zum Zitat Fang Y, Ginsberg C, Seifert M. CKD-induced wingless/integration1 inhibitors and phosphorus cause the CKD-MBD. J Am Soc Nephrol. 2014;25:1760–73. Study provides evidence that injured kidneys may release Wnt antagonists into circulation and that antagonism with neutralizing antibodies can treat low bone disease and vascular calcification. Evidence that aberrant Wnt signaling in endocrine cells is associated with vascular calcification.CrossRefPubMed Fang Y, Ginsberg C, Seifert M. CKD-induced wingless/integration1 inhibitors and phosphorus cause the CKD-MBD. J Am Soc Nephrol. 2014;25:1760–73. Study provides evidence that injured kidneys may release Wnt antagonists into circulation and that antagonism with neutralizing antibodies can treat low bone disease and vascular calcification. Evidence that aberrant Wnt signaling in endocrine cells is associated with vascular calcification.CrossRefPubMed
29.••
Zurück zum Zitat Liu S, Song W, Boulanger JH, et al. Role of TGF-b in a mouse model of high turnover renal osteodystrophy. J Bone Min Res. 2014;29:1141–57. Important study suggesting a role for TGFβ involvement in early pathogenesis of high turnover bone disease.CrossRef Liu S, Song W, Boulanger JH, et al. Role of TGF-b in a mouse model of high turnover renal osteodystrophy. J Bone Min Res. 2014;29:1141–57. Important study suggesting a role for TGFβ involvement in early pathogenesis of high turnover bone disease.CrossRef
30.
Zurück zum Zitat Janssens K, ten Dijke P, Janssens S, Van Hul W. Transforming growth factor β1 to the bone. Endocr Rev. 2005;26:743–74.CrossRefPubMed Janssens K, ten Dijke P, Janssens S, Van Hul W. Transforming growth factor β1 to the bone. Endocr Rev. 2005;26:743–74.CrossRefPubMed
31.
Zurück zum Zitat Tang Y, Wu X, Lei W, et al. TGF-beta1-induced migration of bone mesenchymal stem cells couples bone resorption with formation. Nat Med. 2009;15:757–65.CrossRefPubMedCentralPubMed Tang Y, Wu X, Lei W, et al. TGF-beta1-induced migration of bone mesenchymal stem cells couples bone resorption with formation. Nat Med. 2009;15:757–65.CrossRefPubMedCentralPubMed
32.
Zurück zum Zitat Alliston T, Choy L, Ducy P, Karsenty G, Derynck R. TGF-beta-induced repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation. EMBO J. 2001;20:2254–72.CrossRefPubMedCentralPubMed Alliston T, Choy L, Ducy P, Karsenty G, Derynck R. TGF-beta-induced repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation. EMBO J. 2001;20:2254–72.CrossRefPubMedCentralPubMed
33.
Zurück zum Zitat Grafe I, Yang T, Alexander S, et al. Excessive transforming growth factor-β signaling is a common mechanism in osteogenesis imperfecta. Nat Med. 2014;20:670–5.CrossRefPubMedCentralPubMed Grafe I, Yang T, Alexander S, et al. Excessive transforming growth factor-β signaling is a common mechanism in osteogenesis imperfecta. Nat Med. 2014;20:670–5.CrossRefPubMedCentralPubMed
34.
Zurück zum Zitat Zhen G, Wen C, Jia X, Li Y, et al. Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis. Nat Med. 2013;19:704–12.CrossRefPubMedCentralPubMed Zhen G, Wen C, Jia X, Li Y, et al. Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis. Nat Med. 2013;19:704–12.CrossRefPubMedCentralPubMed
35.
Zurück zum Zitat Gu X, Wang XF. Signaling cross-talk between TGF-β/BMP and other pathways. Cell Res. 2009;19:71–88.CrossRef Gu X, Wang XF. Signaling cross-talk between TGF-β/BMP and other pathways. Cell Res. 2009;19:71–88.CrossRef
36.
Zurück zum Zitat Qui T, Wu X, Zhang F, et al. TGF-β type II receptor phosphorylates PTH receptor to integrate bone remodeling signaling. Nature Cell Biol. 2010;12:224–34. Qui T, Wu X, Zhang F, et al. TGF-β type II receptor phosphorylates PTH receptor to integrate bone remodeling signaling. Nature Cell Biol. 2010;12:224–34.
37.•
Zurück zum Zitat Nguyen J, Tang SY, Nguyen D, Alliston T. Load regulates bone formation and sclerostin expression through a TGFβ-dependent mechanism. PLoS One. 2013;8:1547–53. Provides mechanistic link between TGFβ and sclerostin regulation. Nguyen J, Tang SY, Nguyen D, Alliston T. Load regulates bone formation and sclerostin expression through a TGFβ-dependent mechanism. PLoS One. 2013;8:1547–53. Provides mechanistic link between TGFβ and sclerostin regulation.
38.•
Zurück zum Zitat Cejka D, Herberth J, Branscum AJ, et al. Sclerostin and Dickkopf-1 in renal osteodystrophy. Clin J Am Soc Nephrol. 2011;6:877–82. First report of elevated sclerostin levels in CKD demonstrating relationship with bone formation rates.CrossRefPubMedCentralPubMed Cejka D, Herberth J, Branscum AJ, et al. Sclerostin and Dickkopf-1 in renal osteodystrophy. Clin J Am Soc Nephrol. 2011;6:877–82. First report of elevated sclerostin levels in CKD demonstrating relationship with bone formation rates.CrossRefPubMedCentralPubMed
39.•
Zurück zum Zitat Pelletier S, Dubourg L, Carlier MC, et al. The relation between renal function and serum sclerostin in adult patients with CKD. Clin J Am Soc Nephrol. 2012;8:819–23. Provides assessment of sclerostin serum expression across all stages of CKD progression. Pelletier S, Dubourg L, Carlier MC, et al. The relation between renal function and serum sclerostin in adult patients with CKD. Clin J Am Soc Nephrol. 2012;8:819–23. Provides assessment of sclerostin serum expression across all stages of CKD progression.
40.
Zurück zum Zitat Viaene L, Behets GJ, Claes K, et al. Sclerostin: another bone-related protein related to all-cause mortality in haemodialysis? Dephrol Dial Transplant. 2013;28:3024–30.CrossRef Viaene L, Behets GJ, Claes K, et al. Sclerostin: another bone-related protein related to all-cause mortality in haemodialysis? Dephrol Dial Transplant. 2013;28:3024–30.CrossRef
41.•
Zurück zum Zitat Malluche HH, Davenport DL, Cantor T, Monier-Faugere M-C. Bone mineral density and serum biochemical predictors of bone loss in patients with CKD on dialysis. Clin J Am Soc Nephrol. 2014;9:1254–62. Prospective study examining the relationship over time between serum sclerostin and bone mass. Malluche HH, Davenport DL, Cantor T, Monier-Faugere M-C. Bone mineral density and serum biochemical predictors of bone loss in patients with CKD on dialysis. Clin J Am Soc Nephrol. 2014;9:1254–62. Prospective study examining the relationship over time between serum sclerostin and bone mass.
42.•
Zurück zum Zitat Drechsler C, Evenepoel P, Vervloet MG, et al. High levels of circulating sclerostin are associated with better cardiovascular survival in incident dialysis patients: results from the NECOSAD study. Nephrol Dial Transplant. 2014;0:1–6. Largest prospective study to date examining relationship between serum sclerostin and cardiovascular events. Drechsler C, Evenepoel P, Vervloet MG, et al. High levels of circulating sclerostin are associated with better cardiovascular survival in incident dialysis patients: results from the NECOSAD study. Nephrol Dial Transplant. 2014;0:1–6. Largest prospective study to date examining relationship between serum sclerostin and cardiovascular events.
43.
Zurück zum Zitat Thambiah S, Roplekar R, Manghat P, et al. 2012; Circulating sclerostin and dickkopf1 (DKK1) in predialysis chronic kidney disease (CKD): relationship with bone density and arterial stiffness. Calcif Tissue Int. 2012;90:473–80.CrossRefPubMed Thambiah S, Roplekar R, Manghat P, et al. 2012; Circulating sclerostin and dickkopf1 (DKK1) in predialysis chronic kidney disease (CKD): relationship with bone density and arterial stiffness. Calcif Tissue Int. 2012;90:473–80.CrossRefPubMed
44.
Zurück zum Zitat Claes KJ, Viaene L, Heye S, et al. Sclerostin: another vascular calcification inhibitor? J Clin Endocrin Metab. 2013;98:3221–8.CrossRef Claes KJ, Viaene L, Heye S, et al. Sclerostin: another vascular calcification inhibitor? J Clin Endocrin Metab. 2013;98:3221–8.CrossRef
45.
Zurück zum Zitat De Oliveira RB, Graciolli FG, dos Reis LM, et al. Disturbances of Wnt/β-catenin pathway and energy metabolism in early CKD: effect of phosphate binders. Nephrol Dial Transplant. 2013;28:2510–7.CrossRefPubMed De Oliveira RB, Graciolli FG, dos Reis LM, et al. Disturbances of Wnt/β-catenin pathway and energy metabolism in early CKD: effect of phosphate binders. Nephrol Dial Transplant. 2013;28:2510–7.CrossRefPubMed
46.
Zurück zum Zitat Isakova T Circulating sclerostin as a marker of bone health and disease. Presented at the American Society of Nephrology, Philadelphia, PA, 2014. Isakova T Circulating sclerostin as a marker of bone health and disease. Presented at the American Society of Nephrology, Philadelphia, PA, 2014.
47.
Zurück zum Zitat McNulty M, Singh RJ, Li X. et al. Determination of serum and plasma sclerostin concentrations by enzyme-linked immunoassays. J Clin Endocrinol Metab. 2011;96:E11159-62. McNulty M, Singh RJ, Li X. et al. Determination of serum and plasma sclerostin concentrations by enzyme-linked immunoassays. J Clin Endocrinol Metab. 2011;96:E11159-62.
48.
Zurück zum Zitat Costa AG, Cremers S, Dworakowski E, et al. Comparison of two commercially available ELISAs for circulating sclerostin. Osteoporos Int. 2014;25:1547–54.CrossRefPubMed Costa AG, Cremers S, Dworakowski E, et al. Comparison of two commercially available ELISAs for circulating sclerostin. Osteoporos Int. 2014;25:1547–54.CrossRefPubMed
49.
Zurück zum Zitat Bonani M, Rodriguez D, Fehr T, et al. Sclerostin blood levels before and after kidney transplantation. Kidney Blood Press Res. 2014;39:230–9.CrossRefPubMed Bonani M, Rodriguez D, Fehr T, et al. Sclerostin blood levels before and after kidney transplantation. Kidney Blood Press Res. 2014;39:230–9.CrossRefPubMed
50.
Zurück zum Zitat Arasu A, Cawthon PM, Lui LY, et al. Serum sclerostin and risk of hip fracture in older Caucasian women. J Clin Endocrinol Metab. 2012;97:2027–32.CrossRefPubMedCentralPubMed Arasu A, Cawthon PM, Lui LY, et al. Serum sclerostin and risk of hip fracture in older Caucasian women. J Clin Endocrinol Metab. 2012;97:2027–32.CrossRefPubMedCentralPubMed
51.
Zurück zum Zitat Ardawi MS, Rouzi AA, Al-Sibiani SA. High serum sclerostin predicts the occurrence of osteoporotic fractures in postmenopausal women: the Center of Excellence for Osteoporosis Research Study. J Bone Miner Res. 2012;27:2592–602.CrossRefPubMed Ardawi MS, Rouzi AA, Al-Sibiani SA. High serum sclerostin predicts the occurrence of osteoporotic fractures in postmenopausal women: the Center of Excellence for Osteoporosis Research Study. J Bone Miner Res. 2012;27:2592–602.CrossRefPubMed
52.
Zurück zum Zitat Ardawi MS1, Akhbar DH, Alshaikh A, et al., Increased serum sclerostin and decreased serum IGF-1 are associated with vertebral fractures among postmenopausal women with type-2 diabetes. Bone. 2013;56:355–62. Ardawi MS1, Akhbar DH, Alshaikh A, et al., Increased serum sclerostin and decreased serum IGF-1 are associated with vertebral fractures among postmenopausal women with type-2 diabetes. Bone. 2013;56:355–62.
53.
Zurück zum Zitat Yamamoto M, Yamauchi M, Sugimoto T. Elevated sclerostin levels are associated with vertebral fractures in patients with type 2 diabetes mellitus. J Clin Endocrinol Metab. 2013;98:4030–7.CrossRefPubMed Yamamoto M, Yamauchi M, Sugimoto T. Elevated sclerostin levels are associated with vertebral fractures in patients with type 2 diabetes mellitus. J Clin Endocrinol Metab. 2013;98:4030–7.CrossRefPubMed
54.
Zurück zum Zitat Steitz SA, Speer MY, Curinga G, et al. Smooth muscle cell phenotypic transition associated with calcification. Circ Res. 2001;89:1147–54.CrossRefPubMed Steitz SA, Speer MY, Curinga G, et al. Smooth muscle cell phenotypic transition associated with calcification. Circ Res. 2001;89:1147–54.CrossRefPubMed
55.
Zurück zum Zitat Shao JS, Cheng SL, Pingsterhaus JM, et al. Msx2 promotes cardiovascular calcification by activating paracrine Wnt signals. J Clin Invest. 2005;115:1210–20.CrossRefPubMedCentralPubMed Shao JS, Cheng SL, Pingsterhaus JM, et al. Msx2 promotes cardiovascular calcification by activating paracrine Wnt signals. J Clin Invest. 2005;115:1210–20.CrossRefPubMedCentralPubMed
Metadaten
Titel
Sclerostin and CKD-MBD
verfasst von
Susan C. Schiavi
Publikationsdatum
01.06.2015
Verlag
Springer US
Erschienen in
Current Osteoporosis Reports / Ausgabe 3/2015
Print ISSN: 1544-1873
Elektronische ISSN: 1544-2241
DOI
https://doi.org/10.1007/s11914-015-0263-2

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