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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.

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

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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The information about "RENOPROTECT" are provided by the European Opendata Portal: CORDIS opendata.

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