About this Research Topic
The transmembrane protein Klotho shares homology with glycosidases, and was originally described as an anti-aging factor. There is now ample evidence that transmembrane Klotho functions as an obligatory co-receptor for FGF23 signaling. However, Klotho circulates in the blood stream also as a soluble form lacking the transmembrane domain. Whether soluble Klotho has FGF23 independent effects as a hormone or as a glycosidase remains to be a controversial issue.
The purpose of this Research Topic is to address some of the unresolved questions in this rapidly expanding field, drawing a comprehensive picture of the current state of the art. Current key questions are: How is FGF23 secretion controlled? What is the relative contribution of the four different FGF receptors in FGF23 signaling in different organ systems? What is the interrelationship between FGF23 and the immune system? What is the mechanistic basis for the strong association between circulating FGF23 and heart hypertrophy as well as disease progression in patients with chronic kidney disease? Is there a role of FGF23 in cardiovascular diseases in general? What is the pathophysiological relevance of FGF23 as auto-/paracrine inhibitor of bone mineralization? How can circulating concentrations of soluble Klotho be measured in a reliable fashion? What is the mechanism of action of soluble Klotho, and what is its role in health and disease?
This Research Topic is dedicated to shed more light on these questions and to foster the advancement of the field by combining molecular, animal experimental, and clinical points of view.
Keywords: Fibroblast growth factor-23, Klotho, Mineral metabolism, Heart hypertrophy, Chronic kidney disease
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.