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RENOPROTECT SIGNED

Targeting tubular reabsorption for kidney protection

Total Cost €

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EC-Contrib. €

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Partnership

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 RENOPROTECT project word cloud

Explore the words cloud of the RENOPROTECT project. It provides you a very rough idea of what is the project "RENOPROTECT" about.

glomerulus    validate    nanoparticle    chronic    damage    variants    protein    homeostasis    monoallelic    repair    expression    diagnosis    mice    vulnerable    tubule    combine    featured    first    metabolic    leads    proteinuric    signatures    fitness    applicable    tissues    human    paradigm    dysfunction    evolutionary    downstream    translational    demand    inclusion    lumen    beneficial    disease    forms    experimental    proteinuria    mechanisms    gene    kidney    hypothesis    tolerated    functionally    balancing    humans    specialized    haplotypes    resistance    hypothesize    urine    lies    cubilin    receptor    cell    albuminuria    diabetic    prognosis    explore    renal    partial    encoded    humanized    genetic    ptcs    variability    overload    model    cells    cubn    altogether    cryptic    despite    albumin    proximal    integrative    many    locus    mechanism    genetics    protection    treatment    safe    ptc    drosophila    advantage    relevance    tubular    shows    evolution    reabsorption    mutations    exon    tissue   

Project "RENOPROTECT" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITATSKLINIKUM HEIDELBERG 

Organization address
address: IM NEUENHEIMER FELD 672
city: HEIDELBERG
postcode: 69120
website: www.klinikum.uni-heidelberg.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Total cost 1˙945˙250 €
 EC max contribution 1˙945˙250 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-08-01   to  2025-07-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITATSKLINIKUM HEIDELBERG DE (HEIDELBERG) coordinator 1˙945˙250.00

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 Project objective

Many forms of chronic kidney disease are featured by the loss of protein into the urine (proteinuria). When the cause of proteinuria lies within the glomerulus, such as in diabetic kidney disease, then the protein overload in the tubular lumen may lead to damage of the downstream tubular cells. Particularly vulnerable are proximal tubular cells (PTCs), because these cells are specialized in protein reabsorption and have a high metabolic demand. Dysfunction of the main albumin uptake receptor cubilin (encoded by the CUBN gene) leads to the reduction of albumin uptake and albuminuria. Here, we hypothesize that genetic variants in CUBN are key for providing a cell-to-cell variability that is beneficial for PTC homeostasis and resistance against proteinuric kidney disease. This hypothesis is based on our recent findings that 1.) CUBN mutations are well tolerated by humans despite their proteinuric effects and that 2.) the CUBN locus shows signatures of balancing selection during human evolution. To address this hypothesis, we will first functionally validate common CUBN variants and haplotypes in a humanized Drosophila model and test whether they provide protection against renal disease in mice. Second, we will explore monoallelic CUBN expression and partial cryptic exon inclusion as two possible genetic mechanisms by which CUBN variants could promote proximal tubule fitness and tissue repair. Finally, taking advantage of cubilin dysfunction as a “safe” means to avoid PTC overload, we will target PTC protein uptake in proteinuric mice with the help of a nanoparticle delivery method. Altogether, our integrative translational approach will combine human genetics and experimental studies to explore a new mechanism of proximal tubule homeostasis that may also be applicable to other tissues. Based on evolutionary genetics, we aim to establish a novel paradigm for kidney protection with high relevance for the diagnosis, prognosis and treatment of proteinuric kidney disease.

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