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Título : Role of the RANK/RANKL/OPG and Wnt/β-Catenin Systems in CKD Bone and Cardiovascular Disorders
Autor : Carrilo López, Natalia
Martínez Arias, Laura
Fernández Villabrille, Sara
Ruíz Torres, María Piedad
Dusso, Adriana
Cannata Andía, Jorge B.
Naves Diaz, Manuel
Panizo, Sara
Palabras clave : Klotho
Wnt/β-catenin pathway
Fecha de publicación : abr-2021
Citación : 10.1007/s00223-020-00803-2
Resumen : In the course of chronic kidney disease (CKD), alterations in the bone-vascular axis augment the risk of bone loss, fractures, vascular and soft tissue calcification, left ventricular hypertrophy, renal and myocardial fibrosis, which markedly increase morbidity and mortality rates. A major challenge to improve skeletal and cardiovascular outcomes in CKD patients requires a better understanding of the increasing complex interactions among the main modulators of the bone-vascular axis. Serum Parathyroid hormone (PTH), phosphorus (P), calcium (Ca), fibroblast growth factor 23 (FGF23), calcidiol, calcitriol and Klotho are involved in this axis interact with RANK/RANKL/OPG system and the Wnt/β- catenin pathway. The RANK/RANKL/OPG system controls bone remodelling by inducing osteoblast synthesis of RANKL and downregulating OPG production and it is also is implicated in vascular calcification. The complexity of this system has recently increased due the discovery of LGR4, a novel RANKL receptor involved in bone formation, but possibly also in vascular calcification. The Wnt/β-catenin pathway plays a key role in bone formation, when this pathway is activated bone is formed, when it is inhibited, bone formation is stopped. In the progression of CKD, a downregulation of the Wnt/β-catenin pathway has been described which occurs mainly through the not coincident elevations of sclerostin, Dickkopf1 (Dkk1) and the secreted Frizzled Related Proteins (sFRPs). This review analyses the interactions of PTH, P, Ca, FGF23, calcidiol, calcitriol and Klotho with the RANKL/RANKL/OPG system and the Wnt/β-catenin, pathway and their implications in bone and cardiovascular disorders in CKD
Descripción : The authors wish to thank Instituto de Salud Carlos III (ISCIII; PI17/00715, PI19/00532, PI20/00753), the ISCIII Retic REDinREN (RD06/0016/1013, RD12/0021/0023, RD16/0009/0017 and RD16/0009/0018), Fondo Europeo de Desarrollo Regional (FEDER), Plan Estatal de I+D+I 2013-2016, Plan de Ciencia, Tecnología e Innovación 2013-2017 y 2018-2022 del Principado de Asturias (GRUPIN14-028, IDI-2018-000152), Fundación Renal Iñigo Álvarez de Toledo (FRIAT), and University of Oviedo. N.C.L. has been supported by FINBA-GRUPIN14-028 and IDI-2018- 000152, L.M.A. by FINBA-ISCIII (PI17/00384), S.F.V. was supported by FINBA-ISCIII (PI17/00715), and S.P. by FINBA-IDI-2018-000152.
URI : https://ria.asturias.es/RIA/handle/123456789/14367
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