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ROAR SIGNED

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

Total Cost €

EC-Contrib. €

Partnership

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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.

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

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 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.	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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