AMD_CNV_HIF

Investigating the role of HIFs in myeloid cells during experimental choroidal neovascularisation

 Coordinatore UNIVERSITY COLLEGE LONDON 

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Malgorzata
Cognome: Kielbasa
Email: send email
Telefono: +44 2 031083064

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 231˙283 €
 EC contributo 231˙283 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2013-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-05-01   -   2016-04-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Malgorzata
Cognome: Kielbasa
Email: send email
Telefono: +44 2 031083064

UK (LONDON) coordinator 231˙283.20

Mappa


 Word cloud

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

neovascularisation    myeloid    vegf    progressive    extracellular    amd    neovascular    cells    bruch    hif    cnv    membrane   

 Obiettivo del progetto (Objective)

'Age-related macular degeneration (AMD) is the commonest cause of blindness in the developed world. AMD is a progressive disorder of the outer retina characterised by the accumulation of extracellular deposits and chronic inflammation at the level of Bruch’s basement membrane. Photoreceptor cell death is the result of progressive (‘geographic’) atrophy of supporting retinal pigment epithelium (RPE), or disruption by pathological neovascularisation that arises from the choroid and penetrates defects in Bruch’s membrane. Choroidal neovascularisation (CNV) develops in response to the up-regulation of multiple pro-angiogenic cytokines, including vascular endothelial growth factor (VEGF), in the context of an abnormal extracellular matrix. The outcome of neovascular AMD can be improved by intraocular delivery of VEGF inhibitors but this is incompletely effective, indicating the involvement of additional parallel pathways or compensatory mechanisms. There is a clear unmet need for more effective treatments. In this fellowship I will investigate the hypothesis that HIF activation in myeloid cells is responsible for neovascular AMD. By defining the role of HIF in myeloid cells in the development of experimental CNV I aim to identify new opportunities to improve the efficacy of therapeutic intervention.'

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