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StopIG SIGNED

Translating fundamental insights in podocyte metabolism and cell cycle regulation: development of a new treatment for Stopping crescentic Immune Glomerulonephritis

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 StopIG project word cloud

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

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Project "StopIG" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

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 France [FR]
 Total cost 150˙000 €
 EC max contribution 150˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-PoC
 Funding Scheme ERC-POC
 Starting year 2019
 Duration (year-month-day) from 2019-09-01   to  2021-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 150˙000.00

Map

 Project objective

Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function, with severe damage of glomeruli, the filtering units of the kidney through glomerular crescent formation (crescentshaped scars) seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure and death within months. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents. Currently RPGN is treated with broad-spectrum immunosuppression causing remission of the immune injury achieved in the majority of patients. Nevertheless, risk of end- stage renal failure at 5 years is still near 30 %, with a number of patients developing chronic kidney disease (CKD). Moreover, such treatments are associated with significant morbidity due to infections and malignancy. ERC-supported efforts in our lab have unravelled local mediators and transcription factors that critically control the tolerance of intrinsic glomerular cells to inflammatory insult. My team has shown that the PPARγ (peroxisome proliferatoractivated receptors gamma) pathway is instrumental in the protection of the inflammatory response during immunecomplex mediated RPGN, in large part through protection of kidney cells, named podocytes. We now plan to move forward to transform this finding from our TARGET-GLOMDIS ERC grant into a clinically effective innovative therapy. We expect to bring original therapeutic effect by preventing podocytes death and dysfunction in addition to promoting anti-inflammatory actions. The STOPIG project represents a unique opportunity to provide proof-of-concept for a new and cost-effective therapy for patients with RPGN based on stimulation of PPARγ with repurposed pioglitazone.

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

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