Pathophysiology of Vascular Calcification and Bone Loss: Linked Disorders of Ageing?

Overview

Journal Nutrients

Date 2021 Nov 27

PMID 34836090

Citations 14

Authors

Jorge B Cannata-Andia

Natalia Carrillo-Lopez

Osvaldo D Messina

Neveen A T Hamdy

Sara Panizo

Serge L Ferrari

The International Osteoporosis Foundation Iof Working Group On Bone And Cardiovascular Diseases

Affiliations

Soon will be listed here.

Abstract

Vascular Calcification (VC), low bone mass and fragility fractures are frequently observed in ageing subjects. Although this clinical observation could be the mere coincidence of frequent age-dependent disorders, clinical and experimental data suggest that VC and bone loss could share pathophysiological mechanisms. Indeed, VC is an active process of calcium and phosphate precipitation that involves the transition of the vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Among the molecules involved in this process, parathyroid hormone (PTH) plays a key role acting through several mechanisms which includes the regulation of the RANK/RANKL/OPG system and the Wnt/ß-catenin pathway, the main pathways for bone resorption and bone formation, respectively. Furthermore, some microRNAs have been implicated as common regulators of bone metabolism, VC, left ventricle hypertrophy and myocardial fibrosis. Elucidating the common mechanisms between ageing; VC and bone loss could help to better understand the potential effects of osteoporosis drugs on the CV system.

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