DMP1 prevents osteocyte alterations, FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease.
Bone
Calcium and phosphate metabolic disorders
Pathogenesis
Journal
Bone research
ISSN: 2095-4700
Titre abrégé: Bone Res
Pays: China
ID NLM: 101608652
Informations de publication
Date de publication:
2019
2019
Historique:
received:
18
12
2018
revised:
14
03
2019
accepted:
20
03
2019
entrez:
3
5
2019
pubmed:
3
5
2019
medline:
3
5
2019
Statut:
epublish
Résumé
During chronic kidney disease (CKD), alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality. The osteocyte protein dentin matrix protein 1 (DMP1) reduces FGF23 and enhances bone mineralization, but its effects in CKD are unknown. We tested the hypothesis that DMP1 supplementation in CKD would improve bone health, prevent FGF23 elevations and minimize consequent adverse cardiovascular outcomes. We investigated DMP1 regulation and effects in wild-type (WT) mice and the Col4a3
Identifiants
pubmed: 31044094
doi: 10.1038/s41413-019-0051-1
pii: 51
pmc: PMC6483996
doi:
Types de publication
Journal Article
Langues
eng
Pagination
12Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK076116
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK101730
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK102815
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK114158
Pays : United States
Déclaration de conflit d'intérêts
V.D. has served as a consultant or received honoraria from Vifor, Luitpold, and grant support from Keryx Biopharmaceuticals and Vifor. M.W. has served as a consultant or received honoraria from Amag, Amgen, Akebia, Ardelyx, Diasorin, Keryx, Luitpold, and Sanofi, and grant support from Shire. The remaining authors have no competing interests.
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