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Targeting tubular reabsorption for kidney protection

Total Cost €


EC-Contrib. €






 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.

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

Project "RENOPROTECT" data sheet

The following table provides information about the project.


Organization address
postcode: 69120

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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 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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