Shiguang Liu

TL;DR: Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization, suggesting a bone-renal axis that is central to guiding proper mineral metabolism.

TL;DR: Data suggest that 1,25(OH)(2)D(3) is an important regulator of FGF23 production by osteoblasts in bone and may be to act as a counterregulatory phosphaturic hormone to maintain phosphate homeostasis in response to vitamin D.

TL;DR: Phex, possibly through the actions of unidentified Phex substrates or other downstream effectors, regulates fgf23 expression as part of a potential hormonal axis between bone and kidney that controls systemic phosphate homeostasis and mineralization.

TL;DR: The results suggest that Fgf23 acts downstream of Phex to cause both the renal and bone phenotypes in Hyp mice, and additional factors, associated with either osteocyte differentiation and/or extracellular matrix, are necessary for Phex deficiency to stimulate F gf23 gene transcription in bone.

TL;DR: Knowing the genetic basis of these hereditary disorders of phosphate homeostasis and studies of their mouse homologues have uncovered a bone-kidney axis and new systems biology that govern bone mineralization, vitamin D metabolism, parathyroid gland function, and renal phosphate handling has a significant impact on the diagnosis and treatment of disorders of bone and mineral metabolism.