| [ Summary ] |
Increasing body of evidence indicates the intimate interaction between bone metabolism and cardiovascular disease. Recently, physiological interactions between osteoclasts and osteoblasts have been unraveled. Receptor activator of nuclear factor kB ligand (RANKL) and RANK have been proposed as key players in this interaction. In addition, osteoprotegerin (OPG), which serves as naturally occurring decoy receptor for RANKL/RANK interaction, has been postulated to be involved in the vascular calcification as well as bone disease such as osteoporosis and metastatic bone disease.
In chronic kidney disease (CKD), high serum levels of FGF 23, phosphaturic hormone produced by osteoblasts and osteocytes, are associated with left ventricular hypertrophy (LVH), cardiovascular events, and death. The associations of FGF23 with LVH in the general population as well as hemodialysis patients have also been reported. A recent report indicated that FGF23 directly induces LVH in vivo independent of klotho. Vascular calcification is highly correlated with cardiovascular morbidity and mortality, and linked to ageing, diabetes and CKD. Many studies demonstrated that serum FGF23 levels are directly linked to vascular calcification in general and aortic calcification in particular. However, there are inconsistent reports showing no association between plasma FGF23 and coronary artery calcification in large cohorts. Whether FGF23 may represent a mediator but not a mere marker for vascular calcification remains an open question and further research will be required to better understand the pathophysiology of FGF23 in the development of vascular disease. |