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Prof Elizabeth Cartwright,
Dr X Wang
Applications accepted all year round
Self-Funded PhD Students Only
About the Project
Our research group is focused on understanding the molecular mechanisms underlying the development and progression of heart failure and in doing so identifying potential new targets for its treatment. Heart failure (HF) currently affects around 1 million people in the UK leading to an annual financial burden on the health services of over £1 billion, and its incidence is rising rapidly. HF has a dismal prognosis, with patients dying from progressive pump failure or ventricular arrhythmias. Hypertension, which affects around 15% of the general population, is strongly associated with heart failure with 80% of HF patients having hypertension.
Over the past few years it has become clear that PMCA1, a calcium transporter which ejects calcium from the cell, is involved in all of the central features of heart failure. Human genome wide association studies have shown a link between PMCA1 and hypertension, which is a common underlying cause for HF as well as with coronary artery disease and myocardial infarction. Our own studies have provided functional evidence of the role of PMCA1 in the development of cardiomyopathy, myocardial infarction, arrhythmias and hypertension.
This PhD project will explore and characterise the mechanisms underlying the key role PMCA1 plays in the diseased cardiovascular system.
Entry Requirements
Candidates are expected to hold (or be about to obtain) a minimum upper second class honours degree (or equivalent) in a biomedical, physiology, pharmacology or related area / subject and preferably a master degree.
How To Apply
For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (https://www.bmh.manchester.ac.uk/study/research/apply/). Informal enquiries may be made directly to the primary supervisor. On the online application form select the appropriate subject title.
For international students, we also offer a unique 4 year PhD programme that gives you the opportunity to undertake an accredited Teaching Certificate whilst carrying out an independent research project across a range of biological, medical and health sciences.
Equality, Diversity and Inclusion
Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website https://www.bmh.manchester.ac.uk/study/research/apply/equality-diversity-inclusion/”
Funding Notes
Applications are invited from self-funded students. This project has a Band 2 fee. Details of our different fee bands can be found on our website (View Website).
References
Wilson, C., Oceandy, D., Neyses, L., Cartwright, E.J. (2017). The plasma membrane calcium ATPases and their role as major new players in human disease. Physiol Rev 97, 1089-1125
Little, R., Zi, M., Hammad, S.K., Nguyen, L., Njegic, A., Kurusamy, S., Prehar, S., Armesilla, A.L., Neyses, L., Austin, C., Cartwright, E.J. (2017). Reduced expression of PMCA1 is associated with increased blood pressure with age which is preceded by remodelling of resistance arteries. Aging Cell 16, 1104-1113.
Mohamed, T.M. A., Abou-Leisa, R., Stafford, N., Maqsood, A., Zi, M., Prehar, S., Baudoin-Stanley, F., Wang, X., Neyses, L., Cartwright, E.J., Oceandy, D. (2016). The plasma membrane calcium ATPase 4 signaling in cardiac fibroblasts mediates cardiomyocyte hypertrophy.
Little, R., Zi, M., Hammad, S.K., Nguyen, L., Njegic, A., Kurusamy, S., Prehar, S., Armesilla, A.L., Neyses, L., Austin, C., Cartwright, E.J. (2017). Reduced expression of PMCA1 is associated with increased blood pressure with age which is preceded by remodelling of resistance arteries. Aging Cell 16, 1104-1113.
Mohamed, T.M. A., Abou-Leisa, R., Stafford, N., Maqsood, A., Zi, M., Prehar, S., Baudoin-Stanley, F., Wang, X., Neyses, L., Cartwright, E.J., Oceandy, D. (2016). The plasma membrane calcium ATPase 4 signaling in cardiac fibroblasts mediates cardiomyocyte hypertrophy.
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