Literature DB >> 16952054

Focal and segmental glomerulosclerosis.

N Daskalakis1, M P Winn.   

Abstract

An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm.

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Year:  2006        PMID: 16952054     DOI: 10.1007/s00018-006-6171-y

Source DB:  PubMed          Journal:  Cell Mol Life Sci        ISSN: 1420-682X            Impact factor:   9.261


  8 in total

1.  TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription.

Authors:  Johannes Schlöndorff; Donato Del Camino; Robert Carrasquillo; Vanessa Lacey; Martin R Pollak
Journal:  Am J Physiol Cell Physiol       Date:  2009-01-07       Impact factor: 4.249

2.  The Gne M712T mouse as a model for human glomerulopathy.

Authors:  Sravan Kakani; Tal Yardeni; Justin Poling; Carla Ciccone; Terren Niethamer; Enriko D Klootwijk; Irini Manoli; Daniel Darvish; Shelley Hoogstraten-Miller; Patricia Zerfas; E Tian; Kelly G Ten Hagen; Jeffrey B Kopp; William A Gahl; Marjan Huizing
Journal:  Am J Pathol       Date:  2012-02-07       Impact factor: 4.307

Review 3.  Physiology and pathophysiology of canonical transient receptor potential channels.

Authors:  Joel Abramowitz; Lutz Birnbaumer
Journal:  FASEB J       Date:  2008-10-21       Impact factor: 5.191

4.  Mutation in the key enzyme of sialic acid biosynthesis causes severe glomerular proteinuria and is rescued by N-acetylmannosamine.

Authors:  Belinda Galeano; Riko Klootwijk; Irini Manoli; MaoSen Sun; Carla Ciccone; Daniel Darvish; Matthew F Starost; Patricia M Zerfas; Victoria J Hoffmann; Shelley Hoogstraten-Miller; Donna M Krasnewich; William A Gahl; Marjan Huizing
Journal:  J Clin Invest       Date:  2007-06       Impact factor: 14.808

5.  PPARgamma agonists inhibit TGF-beta-PKA signaling in glomerulosclerosis.

Authors:  Rong Zou; Gang Xu; Xiao-cheng Liu; Min Han; Jing-jing Jiang; Qian Huang; Yong He; Ying Yao
Journal:  Acta Pharmacol Sin       Date:  2009-12-28       Impact factor: 6.150

6.  Glycoprotein hyposialylation gives rise to a nephrotic-like syndrome that is prevented by sialic acid administration in GNE V572L point-mutant mice.

Authors:  Mitutoshi Ito; Kazushi Sugihara; Tomoya Asaka; Tadashi Toyama; Toru Yoshihara; Kengo Furuichi; Takashi Wada; Masahide Asano
Journal:  PLoS One       Date:  2012-01-13       Impact factor: 3.240

7.  Interaction of RAS activation and lipid disorders accelerates the progression of glomerulosclerosis.

Authors:  Kun-Ling Ma; Jie Ni; Chang-Xian Wang; Jing Liu; Yang Zhang; Yu Wu; Lin-Li Lv; Xiong-Zhong Ruan; Bi-Cheng Liu
Journal:  Int J Med Sci       Date:  2013-09-18       Impact factor: 3.738

8.  Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes.

Authors:  Lídia Ambrus; Attila Oláh; Tamás Oláh; György Balla; Moin A Saleem; Petronella Orosz; Judit Zsuga; Klára Bíró; László Csernoch; Tamás Bíró; Tamás Szabó
Journal:  J Cell Mol Med       Date:  2015-09-25       Impact factor: 5.310

  8 in total

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