Claudins in barrier and transport function—the kidney

详细信息    查看全文

• 作者：Yongfeng Gong ; Jianghui Hou
• 关键词：Tight junction ; Claudin ; Kidney ; Ion channel ; Glomerulus ; Epithelium ; Polarity ; Calcium ; Magnesium ; Kidney stone ; Hypertension
• 刊名：Pflügers Archiv - European Journal of Physiology
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：469
• 期：1
• 页码：105-113
• 全文大小：
• 刊物主题：Human Physiology; Molecular Medicine; Neurosciences; Cell Biology; Receptors;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-2013
• 卷排序：469

文摘

Claudins are discovered to be key players in renal epithelial physiology. They are involved in developmental, physiological, and pathophysiological differentiation. In the glomerular podocytes, claudin-1 is an important determinant of cell junction fate. In the proximal tubule, claudin-2 plays important roles in paracellular salt reabsorption. In the thick ascending limb, claudin-14, -16, and -19 regulate the paracellular reabsorption of calcium and magnesium. Recessive mutations in claudin-16 or -19 cause an inherited calcium and magnesium losing disease. Synonymous variants in claudin-14 have been associated with hypercalciuric nephrolithiasis by genome-wide association studies (GWASs). More importantly, claudin-14 gene expression can be regulated by extracellular calcium levels via the calcium sensing receptor. In the distal tubules, claudin-4 and -8 form paracellular chloride pathway to facilitate electrogenic sodium reabsorption. Aldosterone, WNK4, Cap1, and KLHL3 are powerful regulators of claudin and the paracellular chloride permeability. The lessons learned on claudins from the kidney will have a broader impact on tight junction biology in other epithelia and endothelia.