Role Of Tight Junction In Urinary Ca++ Homeostasis | 3540
Journal of Gastrointestinal & Digestive System
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Calcium nephrolithiasis is a common condition. Family-based genetic linkage studies and genome-wide association studies
(GWASs) have uncovered a run of important candidate genes involved in renal Ca++ disorders and kidney stone diseases.
The susceptible genes include membrane proteins such as NKCC2, ROMK and ClCkb/Barttin that underlie renal salt excretion;
tight junction proteins such as claudin-14, -16 and -19 that underlie renal Ca++ excretion; and the Ca++ sensing receptor (CaSR)
that provides a sensing mechanism for the kidney to regulate salt, water and Ca++ homeostasis. Biological and physiological
analyses have revealed the cellular mechanism for transepithelial Ca++ transport in the kidney that depends on the tight junction
to reabsorb Ca++ through a driving force generated by transepithelial salt gradient via the concerted action of these gene
products. Although the individual pathogenic weight of the susceptible genes in nephrolithiasis remains unclear, perturbation of
their expression or function compromises the different steps within the integrated pathway for Ca++ reabsorption, providing a
physiological basis for diagnosing and managing kidney stone diseases.
Jianghui Hou has completed his Ph.D. at the age of 26 years from the University of Edinburgh School of Medicine (UK) and postdoctoral studies
from Harvard University School of Medicine (US). He was appointed Assistant Professor (tenure track) of Medicine by Washington University St.
Louis School of Medicine (US) since 2009. He has published more than 20 papers in reputed journals and received the Young Investigator Prize of
Chinese Society of Nephrology.
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