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ROAR SIGNED

Role of endocycle in Acute Kidney Injury Response and Chronic Kidney Disease development

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 ROAR project word cloud

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

reporter    entirely    critical    vitro    data    experiments    global    unexplored    deaths    re    chronic    mostly    pathophysiological    drive    human    mild    mechanism    first    endocycles    cycle    unclear    unknown    primary    drives    techniques    risk    cells    reversible    enter    function    mammalian    progression    yap1    repair    public    structured    cell    physiologic    regenerative    damage    models    repeatedly    cultures    pathogenesis    epithelial    lineage    fucci2ar    attributed    renal    carry    basis    relevance    disease    cytokinesis    capacity    acute    suggested    preliminary    variants    endocycle    consisting    health    remnant    phases    describe    tracing    recovery    tecs    view    outcomes    subsequent    alone    totally    injury    kidney    time    substantial    collectively    tissues    aki    tissue    tubular    phenomenon    mediated    transgenic    lethal    million    functional    episodes    contributes    animal    ckd    death    nevertheless   

Project "ROAR" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI FIRENZE 

Organization address
address: Piazza San Marco 4
city: Florence
postcode: 50121
website: http://www.unifi.it

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 Italy [IT]
 Total cost 171˙473 €
 EC max contribution 171˙473 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2019
 Duration (year-month-day) from 2019-09-01   to  2021-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI FIRENZE IT (Florence) coordinator 171˙473.00

Map

 Project objective

Acute kidney injury (AKI) is a global public health concern which results in 1.7 million deaths per year. If not lethal in the acute phase, AKI is considered reversible as suggested by recovery of renal function. However, even mild AKI episodes carry substantial risk of developing subsequent chronic kidney disease (CKD). The pathophysiological basis for this phenomenon remains unclear. Injury and death of tubular cells are recognized as the main factors in the pathogenesis of AKI and functional recovery from AKI was traditionally attributed to the regenerative capacity of tubular epithelial cells (TECs) which are believed to re-enter the cell cycle and repair the damage. Nevertheless, my preliminary data provide evidence that an endocycle-mediated response of remnant TECs may represent a critical mechanism of response to AKI. Endocycles are cell cycle variants consisting of G and S phases alone that repeatedly proceed without cytokinesis and its role in repair of mammalian tissues is mostly unknown and totally unexplored in the kidney. This proposal will be structured into 3 distinct objectives to address: 1. The physiologic relevance of endocycle for kidney function recovery after AKI 2. The role of endocycle in the progression of AKI to CKD; 3. The mechanism by which YAP1 drives endocycle and contributes to CKD development. To this end I will use lineage tracing techniques based on the FUCCI2aR reporter applied in different transgenic animal models of AKI, together with in vitro experiments in human primary cultures of renal tubular cells. Collectively, the outcomes of this proposal are expected to provide an entirely novel view of the kidney’s response to AKI, to further our understanding of the processes that drive CKD following AKI, as well as to describe for the first time endocycle as a critical response mechanism to tissue injury in the mammalian kidney.

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

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lastchecktime (2020-10-24 16:52:10) correctly updated