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Despite the widely known fact that low concentrations of extracellular free calcium can induce parathyroid hormone (PTH) secretion, the molecular mechanisms of such regulation and eventual calcium metabolism are not yet completely understood. The traditional view of calcium homeostasis is believed to be maintained by sensing changes in extracellular calcium in several distinct cell types, to stimulate the secretion of PTH, vitamin D and calcitonin, depending on the requirement of the body. These calciotropic hormones then act on the calcium-translocating cells of the kidney, bone and intestine to restore calcium balance [1]. New insights into calcium homeostasis were gained from a recent study by Imura et al.; the investigators proposed that low extracellular free calcium can induce PTH secretion through the klothoand Na+,K+-adenosine triphosphatase (Na+,K+-ATPase)-dependent process [2]. Na+,K+-ATPase is a highly conserved integral membrane protein and is composed of two subunits, the alpha subunit (∼113 kDa) and a smaller beta subunit (∼35 kDa). The alpha subunit is mostly responsible for ion transport and catalytic activity, while the beta subunit regulates the catalytic activity of the alpha subunit [3,4]. The Na+,K+ATPase is a crucial regulator that helps in maintaining intracellular Na+ and K+ concentrations. It is also involved in creating the transmembrane concentration gradient for substrates that require the Na+ gradient for transport across the membrane. The higher Na+ gradient created by the Na+,K+-ATPase activity has been proposed to drive the transepithelial calcium transport in the choroid plexus and the kidney [2].

Klotho and Na+,K+-ATPase activity: solving the calcium metabolism dilemma?