腎尿細管上皮細胞における電解質輸送体の分子生理学的研究

スポンサーリンク

概要

論文の詳細を見る
Patients with lifestyle-related diseases such as hypertension, diabetes, and hyperlipidemia are at high risk for the pathogenesis of a life-threatening atherosclerotic disease. The elucidation of the mechanism responsible for the pathogenesis can bring about the prevention and the cure of lifestyle-related diseases. We think that abnormal transport of electrolytes in renal tubule is involved in lifestyle-related diseases and renal failure. This review focuses on the regulatory mechanisms of Mg2+ transport pathways in renal tubular cells. Mg2+ filtrated by glomeruli is reabsorbed by transcellular and paracellular pathways in renal epithelial cells. Transient receptor potential melastatin 6 (TRPM6) channel is expressed in the apical membrane and involved in the reabsorption of Mg2+. Cyclosporine A decreased TRPM6 expression and Mg2+ influx, suggesting that the decrease in TRPM6 expression may cause hypomagnesemia. Claudin-16 is expressed in the tight junction (TJ) of the thick ascending limb of Henle and may be involved in the paracellular Mg2+ transport. We found that the phosphorylation of claudin-16 is necessary for its localization on the TJ and claudin-16 is de-phosphorylated in Dahl salt-sensitive (DS) hypertensive rats. In epidemiologic studies, magnesium is the correlate of both systolic and diastolic blood pressure. Dysfunction of claudin-16 may be involved in the salt-sensitive hypertension. Dysfunction of Mg2+ reabsorption in renal tubule may be involved in renal failure and lifestyle-related diseases.

著者

関連論文

スポンサーリンク