Dysregulated autophagy contributes to podocyte damage in Fabry's disease. - Wikidata - wikimedia - TriplyDB

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

http://www.wikidata.org/entity/Q34730562

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Podocyte pathology and nephropathy - sphingolipids in glomerular diseases Fabry nephropathy: a review - how can we optimize the management of Fabry nephropathy?Podocytes degrade endocytosed albumin primarily in lysosomes Pathogenesis of glomerular haematuria.Innate and Adaptive Immune Response in Fabry Disease Urinary Podocyte Loss Is Increased in Patients with Fabry Disease and Correlates with Clinical Severity of Fabry Nephropathy MAP1LC3B overexpression protects against Hermansky-Pudlak syndrome type-1-induced defective autophagy in vitro Autophagy-lysosome pathway associated neuropathology and axonal degeneration in the brains of alpha-galactosidase A-deficient mice.Altered dynamics of a lipid raft associated protein in a kidney model of Fabry disease Modulation of mTOR signaling as a strategy for the treatment of Pompe disease.An emerging molecular understanding and novel targeted treatment approaches in pediatric kidney diseases.Mechanisms and biological functions of autophagy in diseased and ageing kidneys.Autophagy in renal diseases.Monitoring Diabetic Nephropathy by Circulating Gangliosides.Distinct Requirements for Vacuolar Protein Sorting 34 Downstream Effector Phosphatidylinositol 3-Phosphate 5-Kinase in Podocytes Versus Proximal Tubular Cells.Ursolic acid improves podocyte injury caused by high glucose.Copious Podocyturia without Proteinuria and with Normal Renal Function in a Young Adult with Fabry Disease.Increased urinary CD80 excretion and podocyturia in Fabry disease.Pathomechanisms of renal Fabry disease.Translational Aspects of Sphingolipid Metabolism in Renal Disorders.Podocyturia is significantly elevated in untreated vs treated Fabry adult patients.Urine-derived cells: a promising diagnostic tool in Fabry disease patients

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Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

http://www.wikidata.org/entity/Q34730562

description

2013 nî lūn-bûn

@nan

2013 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի մայիսին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

@wuu

name

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

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Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@en

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@nl

type

label

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@ast

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@en

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@nl

prefLabel

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@ast

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@en

Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

@nl

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JOURNAL.PONE.0063506

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Dysregulated autophagy contributes to podocyte damage in Fabry's disease.

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Christine E Kurschat

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Claudia Weitbrecht

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Katja Höpker

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Markus Cybulla

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Moin A Saleem

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Roman-Ulrich Müller

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Susanne Brodesser

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Valerie Bartels

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P2860

Guidelines for the use and interpretation of assays for monitoring autophagy

A block of autophagy in lysosomal storage disorders

Receptor-mediated endocytosis of α-galactosidase A in human podocytes in Fabry disease

Reduction of globotriaosylceramide in Fabry disease mice by substrate deprivation

Autophagy: renovation of cells and tissues

Role of mTOR in podocyte function and diabetic nephropathy in humans and mice.

Differential tissue targeting and pathogenesis of verotoxins 1 and 2 in the mouse animal model.

Enzyme replacement therapy with agalsidase alfa in patients with Fabry's disease: an analysis of registry data.

Enzyme replacement therapy in Fabry disease: a randomized controlled trial.

Common and uncommon pathogenic cascades in lysosomal storage diseases

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Bernhard Schermer

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