哺乳动物硫酸盐转运蛋白 NaS1 和 Sat1 的生理作用。
Physiological roles of mammalian sulfate transporters NaS1 and Sat1.
机构信息
School of Biomedical Sciences, University of Queensland, St. Lucia, QLD 4072, Australia.
出版信息
Arch Immunol Ther Exp (Warsz). 2011 Apr;59(2):113-6. doi: 10.1007/s00005-011-0114-5. Epub 2011 Feb 6.
This review summarizes the physiological roles of the renal sulfate transporters NaS1 (Slc13a1) and Sat1 (Slc26a1). NaS1 and Sat1 encode renal anion transporters that mediate proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria and calcium oxalate urolithiasis. Dysregulation of NaS1 and Sat1 leads to hypersulfaturia, hyposulfatemia and liver damage. Loss of Sat1 leads additionally to hyperoxaluria with hyperoxalemia, nephrocalcinosis and calcium oxalate urolithiasis. These data indicate that the renal anion transporters NaS1 and Sat1 are essential for sulfate and oxalate homeostasis, respectively.
这篇综述总结了肾脏硫酸盐转运体 NaS1（Slc13a1）和 Sat1（Slc26a1）的生理作用。NaS1 和 Sat1 编码肾脏阴离子转运体，介导近端肾小管硫酸盐重吸收，从而调节血液硫酸盐水平。靶向敲除小鼠的 NaS1 和 Sat1 导致低硫酸盐血症和高硫酸盐尿症。Sat1 基因缺失的小鼠还表现出高草酸血症、高草酸尿症和草酸钙尿石症。NaS1 和 Sat1 的失调导致高硫酸盐尿症、低硫酸盐血症和肝损伤。Sat1 的缺失还导致高草酸尿症伴高草酸血症、肾钙质沉着症和草酸钙尿石症。这些数据表明，肾脏阴离子转运体 NaS1 和 Sat1 分别是硫酸盐和草酸盐稳态所必需的。
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