The Molecular Interactions between Filtered Proteins and Proximal Tubular Cells in Proteinuria

被引：40

作者：

Baines, Richard J. ^{[1
]}

Brunskill, Nigel J. ^{[1
]}

机构：

[1] Univ Leicester, Sch Med, Dept Infect Immun & Inflammat, Leicester LE1 9HN, Leics, England

来源：

NEPHRON EXPERIMENTAL NEPHROLOGY | 2008年 / 110卷 / 02期

关键词：

Endocytosis; Nephropathy; Proteinuria; Proximal tubule; Signal transduction;

D O I：

10.1159/000161982

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Proteinuria is associated with progressive chronic kidney disease and poor cardiovascular outcomes. Exposure of proximal tubular epithelial cells to excess proteins leads to the development of proteinuric nephropathy with tubular atrophy, interstitial inflammation and scarring. Numerous signalling pathways are activated in proximal tubular epithelial cells under proteinuric conditions resulting in gene transcription, altered growth and the secretion of inflammatory and profibrotic mediators. Megalin, the proximal tubular scavenger receptor for filtered macromolecules, has intrinsic signalling functions and may also link albumin to growth factor receptor signalling via regulated intramembrane proteolysis. It now seems that endocytosis is not always a prerequisite for albumin-evoked alterations in proximal tubular cell phenotype. Recent evidence shows the presence of other potential receptors for proteins, such as the neonatal Fc receptor and CD36, in the proximal tubular epithelium. Copyright (C) 2008 S. Karger AG, Basel

引用

页码：E67 / E71

页数：5

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