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TARGET GLOMDIS

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Cerrado

Glomerulonephritis and Focal Segmental Glomerulosclerosis as a Model to Investig...

Glomerulonephritis and Focal Segmental Glomerulosclerosis as a Model to Investigate the Link between Inflammation and Kidney Disease From Basic Mechanisms to Clinical Application "Rapidly progressive glomerulonephritis (RPGN) and focal and segmental glomerulosclerosis (FSGS) are severe kidney diseases responsible for irreversible renal failure, which is a major risk factor for mortality. Despite the aggres... ver más

28/02/2018

INSERM

1M€

Presupuesto del proyecto: 1M€

Líder del proyecto

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHER... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2018-02-28 No tenemos la información de la convocatoria

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Características del participante

Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

INSERM

0.00€ | Lider

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Líder del proyecto

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHER... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 1M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto "Rapidly progressive glomerulonephritis (RPGN) and focal and segmental glomerulosclerosis (FSGS) are severe kidney diseases responsible for irreversible renal failure, which is a major risk factor for mortality. Despite the aggressiveness of immunosuppressive protocols applied, treatments against RPGN have limited effectiveness. Similarly, there is no specific treatment for FSGS. We built this research project on novel identification of molecular pathways and markers of pathogenic glomerular epithelial cells (GEC). Although major roles of endothelial activation with immune-mediated insult and imbalance between coagulation and fibrinolysis have been demonstrated, our findings reinforce this paradigm that activation of resident glomerular cells play a key role in disease and extend the concept by examining interactions between surrounding cellular systems. We hypothesize that abnormal activation of G-protein coupled receptors (GPCRs) and EGFR may synergize to switch the phenotype of GECs from healthy to pathological. We propose that coagulation and dysfunction of the capillary barrier, may provide GPCR ligands to receptors present in target cells such as GECs. GPCRs, themselves implicated in GN, are known to transactivate the EGFR. The EGFR has the potential to amplify actions of GPCRs in GECs, leading to cytoskeletal rearrangement, and cell death. We hypothesise that interactions between switched GECs and T cells are essential for the perpetuation of the immuno-inflammatory response in such glomerular diseases, after the potentially groundbreaking discovery that lymphocytes display functional EGFR, sensitive to ligands produced by pathological GECs. Finally, we will harness this knowledge for a better identification of patients at risk of glomerular demolition. Our project should identify complementary therapeutic pathways that could then be targeted on top of current immunosuppressive regiments. We also propose that this approach would be beneficial to FSGS."

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