DIADRUG
Insulin resistance and diabetic nephropathy - development of novel in vivo models for drug discovery
| Coordinatore | HELSINGIN YLIOPISTO
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Finland [FI] |
| Totale costo | 2˙000˙000 € |
| EC contributo | 2˙000˙000 € |
| Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | ERC-2009-StG |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2009 |
| Periodo (anno-mese-giorno) | 2009-11-01 - 2014-10-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
HELSINGIN YLIOPISTO
Organization address
address: YLIOPISTONKATU 4 contact info |
FI (HELSINGIN YLIOPISTO) | hostInstitution | 2˙000˙000.00 |
| 2 |
HELSINGIN YLIOPISTO
Organization address
address: YLIOPISTONKATU 4 contact info |
FI (HELSINGIN YLIOPISTO) | hostInstitution | 2˙000˙000.00 |
Mappa
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Obiettivo del progetto (Objective)
'Up to one third of diabetic patients develop nephropathy, a serious complication of diabetes. Microalbuminuria is the earliest sign of the complication, which may ultimately develop to end-stage renal disease requiring dialysis or a kidney transplant. Insulin resistance and metabolic syndrome are associated with an increased risk for diabetic nephropathy. Interestingly, glomerular epithelial cells or podocytes have recently been shown to be insulin responsive. Further, nephrin, a key structural component of podocytes, is essential for insulin action in these cells. Our novel findings show that adaptor protein CD2AP, an interaction partner of nephrin, associates with regulators of insulin signaling and glucose transport in glomeruli. The results suggest that nephrin and CD2AP are involved, by association with these proteins, in the regulation of insulin signaling and glucose transport in podocytes. We hypothesize that podocytes can develop insulin resistance and that disturbances in insulin response affect podocyte function and contribute to the development of diabetic nephropathy. The aim of this project is to clarify the mechanisms leading to development of insulin resistance in podocytes and to study the association between insulin resistance and the development of diabetic nephropathy. For this we will develop transgenic zebrafish and mouse models by overexpressing/knocking down insulin signaling-associated proteins specifically in podocytes. Further, we aim to identify novel drug leads to treat insulin resistance and diabetic nephropathy by performing high-throughput small molecule library screens on the developed transgenic fish models. The ultimate goal is to find a treatment to combat the early stages of diabetic nephropathy in humans.'