Molecular mechanisms of receptor-mediated endocytosis in the renal proximal tubular epithelium.
Molecular mechanisms of receptor-mediated endocytosis in the renal proximal tubular epithelium.
复制标题
DOI：
10.1155/2010/403272
复制
发表时间：
2010
影响因子：
--
通讯作者：
Takeda T
中科院分区：
文献类型：
--
作者：
Saito A;Sato H;Iino N;Takeda T
受体介导的内吞作用是肾近端小管上皮细胞（PTECs）重吸收和代谢肾小球内大量蛋白质和其他物质的关键功能。该功能解释了通过肾小球过滤的营养物质的保存，包括载体结合的维生素和微量元素。该过程的受损导致这些物质的损失和蛋白尿的发展，蛋白尿是肾脏疾病的重要临床体征和心血管疾病的风险标志。Megalin是一种多配体内吞受体，在PTEC的网格蛋白包被的凹坑中表达，在该过程中发挥核心作用。Megalin与各种膜分子合作，并与许多细胞内衔接蛋白相互作用以进行内吞运输。巨蛋白还参与细胞中的信号传导途径。Megalin介导的内吞过载导致PTEC的损伤。需要进一步的研究来阐明megalin介导的内吞作用的机制，并制定预防PTEC损伤的策略。
Receptor-mediated endocytosis is a pivotal function of renal proximal tubule epithelial cells (PTECs) to reabsorb and metabolize substantial amounts of proteins and other substances in glomerular filtrates. The function accounts for the conservation of nutrients, including carrier-bound vitamins and trace elements, filtered by glomeruli. Impairment of the process results in a loss of such substances and development of proteinuria, an important clinical sign of kidney disease and a risk marker for cardiovascular disease. Megalin is a multiligand endocytic receptor expressed at clathrin-coated pits of PTEC, playing a central role in the process. Megalin cooperates with various membrane molecules and interacts with many intracellular adaptor proteins for endocytic trafficking. Megalin is also involved in signaling pathways in the cells. Megalin-mediated endocytic overload leads to damage of PTEC. Further studies are needed to elucidate the mechanism of megalin-mediated endocytosis and develop strategies for preventing the damage of PTEC.
登录
查看更多内容
影响因子：
30.8
作者：
Aminoff, M;Carter, JE;Krahe, R
通讯作者：
Krahe, R
影响因子：
20.3
作者：
Fyfe, JC;Madsen, M;Moestrup, SK
通讯作者：
Moestrup, SK
影响因子：
13.6
作者：
Coudroy, G;Gburek, J;Maurice, M
通讯作者：
Maurice, M
影响因子：
16.2
作者：
Hong, CY;Hughes, K;Ling, SL
通讯作者：
Ling, SL
影响因子：
--
作者：
AVISSAR, N;ORNT, DB;COHEN, HJ
通讯作者：
COHEN, HJ