A new approach to treating pulmonary arterial hypertension
Professor Andrew Howard Baker (lead researcher)
University of Edinburgh
Start date: 01 January 2013 (Duration 3 years)
Development of MIR-145 antagonism as a novel therapeutic strategy for application to the treatment of pulmonary arterial hypertension
Pulmonary arterial hypertension (PAH) involves overactive cell growth in blood vessel walls which reduces the space for blood flow in the lungs. PAH symptoms include breathlessness and chest pain. The signs worsen as lung blood pressure increases, and the disorder is often fatal. Although there are treatments available, they are often not effective. A University of Glasgow team led by BHF Professor Andrew Baker and Professor Margaret MacLean has recently made an exciting discovery in our understanding of PAH. They have found that certain pieces of micro-RNA (miRNA) - tiny molecules that control the activity of our genes - may play a crucial role in the development of PAH. In mice, they found that the amount of one particular miRNA, called miRNA145, is higher in lungs affected by PAH. This latest award to the Glasgow team will clarify the role of miRNA145 in PAH, leading to a better understanding of the disease and possibly to future treatments. Using mice and rats, the scientists will look at the effect of switching off miRNA145 in the lungs to see if it could have a beneficial effect. As one type of miRNA can have an effect on many genes, a future therapy based on changing ‘normal’ levels of miRNA could make a big difference in patients with PAH. This work on understanding the causes of PAH takes place alongside other programmes led by Professor Baker, which are looking at the possibility of using miRNAs and whole genes to treat heart patients, including improving results for patients who have had coronary bypass surgery.
Project details
Grant amount | £476,060 |
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Grant type | Chairs & Programme Grants |
Application type | Special Project |
Start Date | 01 January 2013 |
Duration | 3 years |
Reference | SP/12/9/29593 |
Status | Complete |