Why is pulmonary arterial hypertension more common in women?
Professor Margaret MacLean (lead researcher)
University of Glasgow
Start date: 01 October 2011 (Duration 5 years)
Gender and the development of pulmonary arterial hypertension
Pulmonary arterial hypertension is a rare but fatal disorder of high blood pressure in the blood vessels that supply the lungs. The condition is caused by the narrowing of these vessels. Although treatments are available, they are not fully effective. The condition causes symptoms including shortness of breath, and affects more women than men. This team, led by Professor Mandy MacLean and including BHF Chairs Andrew Baker (at University of Edinburgh) and Nick Morrell (at the University of Cambridge) aims to find out the reasons behind the gender difference in the development of pulmonary arterial hypertension. Previous research has shown that changes in the way the body makes and breaks down the hormone oestrogen might be involved in the development of the disease. Other hormones such as serotonin also seem to be involved, and a faulty gene called BMPR2 is also known to be a factor in some cases. This major research programme aims to bring all these clues together, painting a more accurate picture of what causes pulmonary arterial hypertension in women. Using mice, the researchers will look at the combined effects of oestrogen, serotonin and BMPR2 in the development of the disease. This group has expertise in studying miRNAs, tiny pieces of genetic material that regulate which of your genes are switched ‘on’ or ‘off’. The ability of blood vessel cells in the lungs to make the right miRNAs to control blood pressure is another key factor in the development of pulmonary arterial hypertension. By leading to greater understanding of the disease, the research could point the way to future treatments.
Project details
Grant amount | £974,293 |
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Grant type | Chairs & Programme Grants |
Application type | Programme Grant |
Start Date | 01 October 2011 |
Duration | 5 years |
Reference | RG/11/7/28916 |
Status | Complete |