Critical Bridge Between Bone Metabolism and Cardiovascular Disease
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Parathyroid hormone (PTH) is a principal regulator of calcium balance in physiological and pathological conditions associated with cardiovascular disorders and plays a major physiological role in bone homeostasis (Figure 1). PTH systemically controls bone remodeling by modulating the bone marrow microenvironment and regulating osteogenic signaling pathways.1 PTH and its related peptide can have both anabolic and catabolic effects. Although intermittent administration of PTH is osteoanabolic and antiosteoporotic via stimulation of bone formation, its continuous administration may cause catabolic osteoporotic changes. Experimental studies showed that intermittent injection of full length PTH (PTH1–84) or its N-terminal fragment (PTH1–34) increases bone formation with normal microarchitecture by coupling bone remodeling1 as well as promoting bone vascular structure and function.2 Clinically, intermittent administration of PTH is an established osteoanabolic therapy that improves quality of life in patients with severe osteoporosis.3 However, potential adverse effects by long-term use of PTH have not been fully elucidated.
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The presence of PTH receptors within the cardiovascular system,4 including vasculature (smooth muscle cells, endothelial cells) and heart (cardiomyocytes), suggests that secreted PTH may play a role in the pathophysiology of cardiovascular diseases beyond its role in mineral and bone metabolism (Figure 2).