Literature DB >> 12915777

Podocyte biology and the emerging understanding of podocyte diseases.

Laura Barisoni1, Peter Mundel.   

Abstract

The understanding of the unique molecular apparatus of the podocyte has increased dramatically in recent years. This new knowledge has improved the diagnosis and classification of the diseases that have been termed podocytopathies. Podocyte injury frequently leads to reorganization of the slit diaphragm and reorganization of the foot process structure. Four major causes of foot process effacement can be identified, with some due to genetic mutations and others due to acquired conditions: (1) impaired formation of the slit diaphragm complex; (2) abnormalities of the glomerular basement membrane or the adhesion of podocytes to the glomerular basement membrane; (3) abnormalities of the actin cytoskeleton and associated proteins, and (4) alterations in the apical membrane domain of the podocyte. The major podocytopathies can also be organized into four categories, including those with a normal glomerular histology, diffuse mesangial sclerosis, focal segmental glomerulosclerosis, and collapsing glomerulopathy. Copyright 2003 S. Karger AG, Basel

Entities:  

Mesh:

Year:  2003        PMID: 12915777     DOI: 10.1159/000072917

Source DB:  PubMed          Journal:  Am J Nephrol        ISSN: 0250-8095            Impact factor:   3.754


  36 in total

1.  Rho activation of mDia formins is modulated by an interaction with inverted formin 2 (INF2).

Authors:  Hua Sun; Johannes S Schlondorff; Elizabeth J Brown; Henry N Higgs; Martin R Pollak
Journal:  Proc Natl Acad Sci U S A       Date:  2011-01-28       Impact factor: 11.205

Review 2.  TRPC6 in glomerular health and disease: what we know and what we believe.

Authors:  Johannes S Schlöndorff; Martin R Pollak
Journal:  Semin Cell Dev Biol       Date:  2006-11-20       Impact factor: 7.727

3.  Persistent NF-kappaB activation in renal epithelial cells in a mouse model of HIV-associated nephropathy.

Authors:  Scott Martinka; Leslie A Bruggeman
Journal:  Am J Physiol Renal Physiol       Date:  2005-10-04

4.  A maladaptive role for EP4 receptors in podocytes.

Authors:  Erin M Stitt-Cavanagh; Wissam H Faour; Kaede Takami; Anthony Carter; Barbara Vanderhyden; Youfei Guan; Andre Schneider; Matthew D Breyer; Christopher R J Kennedy
Journal:  J Am Soc Nephrol       Date:  2010-07-29       Impact factor: 10.121

5.  Ginsenoside Rg1 protects mouse podocytes from aldosterone-induced injury in vitro.

Authors:  Nan Mao; Yuan Cheng; Xin-li Shi; Li Wang; Ji Wen; Qiong Zhang; Qiong-dan Hu; Jun-ming Fan
Journal:  Acta Pharmacol Sin       Date:  2014-03-17       Impact factor: 6.150

6.  Math6 expression during kidney development and altered expression in a mouse model of glomerulosclerosis.

Authors:  Michael D Ross; Scott Martinka; Amitava Mukherjee; John R Sedor; Charles Vinson; Leslie A Bruggeman
Journal:  Dev Dyn       Date:  2006-11       Impact factor: 3.780

7.  Estrogen receptor subtype ratio change protects against podocyte damage.

Authors:  Paola Catanuto; Xiaomei Xia; Simone Pereira-Simon; Sharon Elliot
Journal:  Curr Trends Endocinol       Date:  2017

8.  Glomerular angiotensinogen is induced in mesangial cells in diabetic rats via reactive oxygen species--ERK/JNK pathways.

Authors:  Naro Ohashi; Maki Urushihara; Ryousuke Satou; Hiroyuki Kobori
Journal:  Hypertens Res       Date:  2010-08-05       Impact factor: 3.872

9.  In vivo 17β-estradiol treatment contributes to podocyte actin stabilization in female db/db mice.

Authors:  Paola Catanuto; Alessia Fornoni; Simone Pereira-Simon; Fayi Wu; Kerry L Burnstein; Xiaomei Xia; Francesco Conti; Andrea Lenzi; Sharon Elliot
Journal:  Endocrinology       Date:  2012-10-15       Impact factor: 4.736

10.  Reduced podocin expression in minimal change disease and focal segmental glomerulosclerosis is related to the level of proteinuria.

Authors:  Vinita Agrawal; Narayan Prasad; Manoj Jain; Rakesh Pandey
Journal:  Clin Exp Nephrol       Date:  2013-02-02       Impact factor: 2.801

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.