Molecular Physiology Group, School of Biomedical Sciences, Univ. of Queensland, St. Lucia, Australia.
Am J Physiol Renal Physiol. 2011 Jun;300(6):F1267-70. doi: 10.1152/ajprenal.00061.2011. Epub 2011 Apr 13.
This review will briefly summarize current knowledge on the renal anion transporters sodium-sulfate cotransporter-1 (NaS1; Slc13a1) and sulfate-anion transporter-1 (Sat1; Slc26a1). NaS1 and Sat1 mediate renal proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Sat1 also mediates renal oxalate transport and controls blood oxalate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria, and calcium oxalate urolithiasis. NaS1 and Sat1 null mice also have other phenotypes that result due to changes in blood sulfate and oxalate levels. Experimental data indicate that NaS1 is essential for maintaining sulfate homeostasis, whereas Sat1 controls both sulfate and oxalate homeostasis in vivo.
这篇综述将简要总结目前关于肾阴离子转运体钠-硫酸盐共转运蛋白 1（NaS1；Slc13a1）和硫酸盐阴离子转运体 1（Sat1；Slc26a1）的知识。NaS1 和 Sat1 介导肾近端小管硫酸盐重吸收，从而调节血液硫酸盐水平。Sat1 还介导肾草酸转运，控制血液草酸盐水平。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 基因敲除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 基因敲除小鼠还存在其他表型，这是由于血液硫酸盐和草酸盐水平的变化所致。实验数据表明，NaS1 对维持硫酸盐稳态至关重要，而 Sat1 则在体内控制硫酸盐和草酸盐稳态。
