Phosphate is essential for proper cell function by providing the fundamentals for DNA, cellular structure, signaling and energy production. The homeostasis of phosphate is regulated by the phosphaturic hormones fibroblast growth factor (FGF) 23 and parathyroid hormone (PTH). Recent studies indicate that phosphate induces phosphate sensing mechanisms via binding to surface receptors and phosphate cotransporters leading to feedback loops for additional regulation of serum phosphate concentrations as well as by phosphate itself. An imbalance to either side, enhances or reduces serum phosphate levels, respectively. The latter is associated with increased risk for cardiovascular diseases and mortality. Hyperphosphatemia is often due to impaired kidney function and linked to vascular disease, hypertension and left ventricular hypertrophy. In contrast, hypophosphatemia either due to reduced dietary intake or intestinal absorption of phosphate or hereditary or acquired renal phosphate wasting, may result in impaired energy metabolism and cardiac arrhythmias. Here, we review the effects and its underlying mechanisms of deregulated serum phosphate concentrations on the cardiovascular system. Finally, we summarize the current therapeutic approaches for both lowering serum phosphate levels and improvement of cardiovascular disease.
Keywords: Fibroblast growth factor 23; Intervention; Left ventricular hypertrophy; Parathyroid hormone; Phosphate; Vascular disease.
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