EU H2020 Project "STOPIG (Translating fundamental insights in podocyte metabolism and cell cycle..)": description, partecipants, costs and EC-fundings

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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.

immunosuppression podocytes insult transcription cells near anti risk stage scars grant mediators chronic preventing stimulation original mediated lab ppar rapid protection function causing innovative glomerulonephritis proof crescent nevertheless injury malignancy transform therapy team remission receptors patients named months filtering repurposed opportunity glomeruli gamma majority infections renal kidney pioglitazone containing immunecomplex glomdis local therapeutic ckd immune plan units crescents biopsies crescentshaped stopig peroxisome underlying damage disease treatments left morbidity regardless unravelled glomerular severe tolerance syndrome efforts rapidly progressive effect move progresses death dysfunction kidneys intrinsic critically untreated clinically erc broad acute rpgn shown inflammatory proliferatoractivated actions instrumental spectrum

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

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

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE

FR (PARIS)

coordinator

150˙000.00

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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