BP-CARDIO

"Investigating the therapeutic potential of manipulating the IGF-IGFBP1 axis in the prevention and treatment of cardiovascular disease, diabetes and obesity."

 Coordinatore UNIVERSITY OF LEEDS 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 1˙493˙543 €
 EC contributo 1˙493˙543 €
 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-2012-StG_20111109
 Funding Scheme ERC-SG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-01-01   -   2017-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY OF LEEDS

 Organization address address: WOODHOUSE LANE
city: LEEDS
postcode: LS2 9JT

contact info
Titolo: Dr.
Nome: Stephen Bentley
Cognome: Wheatcroft
Email: send email
Telefono: +44 113 3437760

UK (LEEDS) hostInstitution 1˙493˙543.00
2    UNIVERSITY OF LEEDS

 Organization address address: WOODHOUSE LANE
city: LEEDS
postcode: LS2 9JT

contact info
Titolo: Mr.
Nome: Benjamin
Cognome: Williams
Email: send email
Telefono: +44 113 3434934
Fax: +44 113 3430949

UK (LEEDS) hostInstitution 1˙493˙543.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

diabetes    risk    nitric    atherosclerosis    disease    oxide    igf    mice    related    igfbp    prevent    cardiovascular    proteins    endothelial    therapeutic    insulin    bioavailability    resistance    obesity    binding    protective    cells   

 Obiettivo del progetto (Objective)

'More than 30 million people are living with diabetes in the EU, with a prevalence expected to grow to over 10% of the adult population by the year 2030. Type 2 diabetes is a major cause of cardiovascular disease related death and disability, substantially increasing the risk of myocardial infarction, stroke and peripheral arterial disease. Recent landmark trials, showing that intensive glucose control does not improve cardiovascular outcomes and may increase mortality in some circumstances, provide a compelling rationale for intense research aimed at developing novel therapeutic strategies. Type 2 diabetes is underpinned by resistance to the effects of insulin, which I have shown in endothelial cells causes reduced bioavailability of the anti-atherosclerotic molecule nitric oxide and leads to accelerated atherosclerosis. The cellular effects of insulin are mirrored by insulin-like growth factor factor-1, the bioavailability of which at its receptor is in turn is regulated by a family of high affinity binding proteins (IGFBP). Epidemiological studies demonstrate and inverse association between one of these binding proteins, IGFBP1, and diabetes-related cardiovascular risk. I have recently demonstrated that IGFBP1 when expressed in mice can ameliorate insulin resistance, obesity and atherosclerosis. In endothelial cells, I showed that IGFBP1 upregulates the production of nitric oxide indepenedently of IGF. These findings suggest that IGFBP1 may be a ‘protective’ endogenous protein and that increasing circulating levels may be a therapeutic strategy to prevent development of diabetes and cardiovascular disease. In this proposal I will address this hypothesis by employing state of the art studies in cells and novel gene modified mice to unravel the molecular basis of the protective effects of IGFBP1 and to investigate the possibility of exploiting the IGF-IGFBP axis to prevent cardiovascular disease in the setting of diabetes and obesity.'

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