Therapeutic resolution of BMPR2-mediated signalling defects in pulmonary arterial hypertension (PAH)

About the Project

Pulmonary arterial hypertension (PAH) is an incurable and devastating disease and death occurs within 2.5 years of diagnosis. Sustained elevation of the pulmonary arterial pressure (PAP) above 25mm Hg at rest or 30mm Hg during exercise with a normal pulmonary capillary wedge pressure (≤15mm Hg) in the absence of underlying heart, lung or thrombo-occlusive disorders is clinically known as PAH. At present, there is no cure for this disorder.

Current therapies for PAH are very costly with an estimated annual treatment and care expenditure for each PAH patient varying substantially between medications, with £39,000 for iloprost, £23,500 for bosentan, £6,000 for sildenafil and £120,000 for treprostinil with combination therapy potentially reaching an average of a £200-300,000 per year. Therefore, there is an urgent need to develop effective medicines to treat PAH.

We have showed that mutations in a specific gene (called BMPR2) can increase a person's risk of getting PAH and identified factors that regulate the BMPRII-mediated signalling defects in PAH. In this project we will investigate the underlying mechanisms of disease pathogenesis and identify novel therapies for PAH.

How to apply

Formal applications can be submitted through the University of Bradford web site; applicants will need to register an account, select 'Postgraduate Research' as the type of course and then use the keyword 'pharmacy'. Applicants should then specify the project title in the 'Research Proposal' section.

Funding Notes

This is a self-funded project; applicants will be expected to pay their own fees or have access to suitable third-party funding, such as the Doctoral Loan from Student Finance. In addition to the university's standard tuition fees, bench fees may also apply to this project.