UNIVERSITY OF GLASGOW

The University of Glasgow is a leading clinical centre in cardiovascular medicine and vascular biology. The British Heart Foundation, Glasgow Cardiovascular Research Centre (BHF GCRC) is part of the Institute of Cardiovascular and Medical Sciences. It is one of seven Research Institutes within the College of Medical, Veterinary and Life Sciences. The BHF GCRC is one of the UK's top rated Cardiovascular Research Centres and a translational centre of excellence, with a focus on primary and secondary prevention of cardiovascular disease.

Within sysVASC, the University of Glasgow will contribute GWAS and proteomic datasets and samples from large population based cohorts, advanced systems biology approaches including tools for inter-species cross-talk as well as animal models.

© biolution GmbH

Christian Delles, MD

Christian Delles has more than 15 years of experience in cardiovascular phenotyping. He is reader in Cardiovascular Medicine at the University of Glasgow and Honorary Consultant Physician with NHS Greater Glasgow & Clyde. Christian Delles is a member of several other national and international hypertension and renal associations and has more than 110 peer reviewed publications. He has a research interest in cardiovascular risk stratification and has coordinated and been a principal investigator in several EC funded FP7 initiatives.

© University of Glasgow

CONTACT

WEB: gla.ac.uk
EMAIL: Christian.Delles@glasgow.ac.uk

1 Flores- Muñoz, M., et al. (2012) Adenoviral Delivery of Angiotensin-(1-7) or Angiotensin-(1-9) Inhibits Cardiomyocyte Hypertrophy via the Mas or Angiotensin Type 2 Receptor. PLoS One. 7, e45564.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0045564

2 Flores-Muñoz, M., et al. (2012) Angiotensin-(1-9) Attenuates Cardiac Fibrosis in the Stroke-Prone Spontaneously Hypertensive Rat via the Angiotensin Type 2 Receptor. Hypertension. 59, 300-7.
http://hyper.ahajournals.org/content/59/2/300.long

3 Flores- Muñoz M., et al. (2011)Angiotensin1-9 antagonises pro-hypertrophic signalling in cardiomyocytes via the angiotensin type 2 receptor. J Physiol. 589, 939-51.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060371/

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