Podocyte biology in human disease

被引：23

作者：

De Zoysa, JR

Topham, PS

机构：

[1] Auckland City Hosp, Dept Renal Med, Auckland, New Zealand

[2] Univ Leicester, Leicester Gen Hosp, John Walls Renal Unit, Dept Inflammat Infect & Immun, Leicester, Leics, England

来源：

NEPHROLOGY | 2005年 / 10卷 / 04期

关键词：

nephrotic syndrome; podocyte; proteinuria;

D O I：

10.1111/j.1440-1797.2005.00401.x

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：

The podocyte is a highly specialized cell that plays a key role in regulating the glomerular filtration barrier. A number of advances have been made in recent years, linked to the discovery of single-gene defects in hereditary glomerular disease, which highlight the role of this cell in preventing proteinuria. This article reviews the molecular biology of the podocyte, focusing on known genetic abnormalities.

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收藏

页码：362 / 367

页数：6

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[1] NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome [J].

Boute, N ;

Gribouval, O ;

Roselli, S ;

Benessy, F ;

Lee, H ;

Fuchshuber, A ;

Dahan, K ;

Gubler, MC ;

Niaudet, P ;

Antignac, C .

NATURE GENETICS, 2000, 24 (04) :349-354

[2] Inducible gene silencing in podocytes: A new tool for studying glomerular function [J].

Bugeon, L ;

Danou, A ;

Carpentier, D ;

Langridge, P ;

Syed, N ;

Dallman, MJ .

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2003, 14 (03) :786-791

[3] Mutations in LMX1B cause abnormal skeletal patterning and renal dysplasia in nail patella syndrome [J].

Dreyer, SD ;

Zhou, G ;

Baldini, A ;

Winterpacht, A ;

Zabel, B ;

Cole, W ;

Johnson, RL ;

Lee, B .

NATURE GENETICS, 1998, 19 (01) :47-50

[4] A novel adaptor protein orchestrates receptor patterning and cytoskeletal polarity in T-cell contacts [J].

Dustin, ML ;

Olszowy, MW ;

Holdorf, AD ;

Li, J ;

Bromley, S ;

Desai, N ;

Widder, P ;

Rosenberger, F ;

van der Merwe, PA ;

Allen, PM ;

Shaw, AS .

CELL, 1998, 94 (05) :667-677

[5] Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases [J].

Eremina, V ;

Sood, M ;

Haigh, J ;

Nagy, A ;

Lajoie, G ;

Ferrara, N ;

Gerber, HP ;

Kikkawa, Y ;

Miner, JH ;

Quaggin, SE .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (05) :707-716

[6]

Eremina V, 2002, J AM SOC NEPHROL, V13, DOI 10.1681/ASN.V133788

[7] Glomerular expression of nephrin is decreased in acquired human nephrotic syndrome [J].

Furness, PN ;

Hall, LL ;

Shaw, JA ;

Pringle, JH .

NEPHROLOGY DIALYSIS TRANSPLANTATION, 1999, 14 (05) :1234-1237

[8] ALTERNATIVE SPLICING AND GENOMIC STRUCTURE OF THE WILMS-TUMOR GENE-WT1 [J].

HABER, DA ;

SOHN, RL ;

BUCKLER, AJ ;

PELLETIER, J ;

CALL, KM ;

HOUSMAN, DE .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (21) :9618-9622

[9] Two splice variants of the Wilms' tumor 1 gene have distinct functions during sex determination and nephron formation [J].

Hammes, A ;

Guo, JK ;

Lutsch, G ;

Leheste, JR ;

Landrock, D ;

Ziegler, U ;

Gubler, MC ;

Schedl, A .

CELL, 2001, 106 (03) :319-329

[10] Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling [J].

Huber, TB ;

Hartleben, B ;

Kim, J ;

Schmidts, M ;

Schermer, B ;

Keil, A ;

Egger, L ;

Lecha, RL ;

Borner, C ;

Pavenstädt, H ;

Shaw, AS ;

Walz, G ;

Benzing, T .

MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (14) :4917-4928

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