Longevity Articles

Age-Related Blood Vessel Calcification and Bone Loss Share Physiological Mechanisms

Age-Related Blood Vessel Calcification and Bone Loss Share Physiological Mechanisms
  • Vascular calcifications are mineral deposits on the walls of your arteries and veins. These mineral deposits can stick to plaque and fat that are already built up on the walls of a blood vessel.
  • The compound parathyroid hormone (PTH) plays a key role in age-related blood vessel calcification.
  • PTH also interacts with two other pathways that are needed for bone resorption and bone formation, respectively.
  • However, the question remains: what comes first — does bone loss drive the vascular calcification, or is it the other way around?  

A new review elucidates the numerous mechanisms shared by vascular (blood vessel) calcification and age-related bone loss, identifying the following key associations:

  • Vascular calcification 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 include the regulation of the RANK/RANKL/OPG system and the Wnt/ß-catenin pathway, the main pathways for bone resorption and bone formation, respectively. 

Vascular calcification, low bone mass and fragility fractures are all frequent age-dependent disorders. Recent clinical and experimental data suggest that vascular calcification and bone loss could share pathophysiological mechanisms. 

Professor Jorge B. Cannata-Andia, lead author, stated:

“This review consolidates current knowledge on how the pathogenesis and progression of vascular calcification and bone loss share several factors and pathways. This question remains: what comes first  - is bone loss driving the vascular calcification or the opposite? Or, is there a higher level of dysregulation through aging processes that impacts on both tissues simultaneously but through similar mechanisms?”

In its summary and conclusions, the Working Group underscores the fact that the increase or decrease in tissue and/or serum levels of PTH, the RANK/RANKL/OPG system and the Wnt/bcatenin pathways, calcium, phosphate, FGF23, among the most studied factors, may play a pathogenic role but can also be used as markers of bone and heart conditions. However, levels of some serum markers should be interpreted with caution, as the correlation between hormone levels and tissue levels needs to be better investigated. 

Professor Serge Ferrari, Co-chair of the IOF Working Group and Vice-Chair of the IOF Committee of Scientific Advisors, concluded:

“Better understanding of the shared mechanisms between aging, vascular calcification, and bone loss may ultimately help us to better understand the potential effects of [bone loss] drugs on the cardiovascular system. We hope that this review serves to clarify and summarize current knowledge on the pathophysiology of these common mechanisms, as a stepping stone to further research.” 




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