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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

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 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.

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

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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