Abstract

Clinically, vascular calcification is now accepted as a valuable predictor of coronary heart disease.151 Achieving control over this process requires understanding mechanisms in the context of a tightly-controlled regulatory network, with multiple, nested feedback loops and cross-talk between organ systems, in the realm of control theory. Thus, treatments for osteoporosis such as calcitriol, estradiol, bisphosphonates, calcium supplements, and intermittent parathyroid hormone are likely to affect vascular calcification, and, conversely, many treatments for cardiovascular disease such as statins, antioxidants, hormone replacement therapy, ACE inhibitors, fish oils, and calcium channel blockers may affect bone health. As we develop and use treatments for cardiovascular and skeletal diseases, we must give serious consideration to the implications for the organ at the other end of the bone-vascular axis.

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