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Stopping early stage heart disease progressing to heart failure

Dr Viola Kooij (lead researcher)

Imperial College London

Start date: 01 September 2014 (Duration 2 years)

Profilin-1, a critical mediator of cardiac performance

Hundreds of thousands of people are living with heart failure and currently there is no cure. Understanding the changes that occur in early stages of heart disease could reveal new ways to design drugs which stop patients progressing to heart failure. In patients with heart disease, the heart muscle weakens and can no longer effectively pump blood throughout the body. At first, the heart compensates by growing larger - this is called compensated hypertrophy, but the heart can’t maintain this for long and heart failure develops. Lots of changes occur to the heart’s structure during compensated hypertrophy, e.g. cells are bigger and protein levels are altered. Profilin-1 is an important protein that maintains the structural scaffolding of cells but scientists do not clearly understand what it does in the heart. Dr Viola Kooij and her team at Imperial College London have discovered that the heart needs profilin-1 to work properly. They believe it is also important in disease development – there is more profilin-1 in diseased heart muscle cells and it can influence other genes and proteins important in disease. The BHF has now awarded the team a grant to investigate profilin-1’s dual role in healthy and diseased hearts. They will try to confirm how important profilin-1 is in compensated hypertrophy, what profilin-1 does in heart muscle cells and how it is controlled. They will work out if stopping heart muscle cells making more profilin-1 stops the heart getting bigger and if this slows or prevents the development of heart failure. Understanding what this protein does in early heart disease may reveal new ways to prevent heart failure.

Project details

Grant amount £151,612
Grant type Project Grants
Application type Project Grant
Start Date 01 September 2014
Duration 2 years
Reference PG/14/44/30890
Status Complete
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