Postgraduate research 

Cardiovascular & Medical Sciences PhD/iPhD/MD/MSc (Research)

blood cells

Cardiovascular disease is projected to remain the single leading cause of death over the next two decades, accountable for considerable disability and reduction in the quality of life, therefore research is vital to advance its diagnosis, treatment and prevention. Our strength is in identifying and designing novel therapeutic strategies that will lead to clinical trials.

  • PhD: 3-4 years full-time; 5 years part-time;
  • MD (Doctor of Medicine): 2 years full-time; 4 years part-time (for medically-qualified graduates only) part-time;
  • MSc (Research): 1 year full-time; 2 years part-time;

Research projects

Fully-funded PhD opportunities

Self-funded PhD opportunities

+++

Uromodulin a Precision Medicine Target for Novel Drug Discovery in Cardiovascular Disease

Supervisors: Delyth GrahamMartin McBride

Background: Despite major advances in cardiovascular health, hypertension remains the risk factor contributing most to the overall burden of disease globally. When the total global impact of known risk factors on the overall burden of disease is calculated, 54% of stroke and 47% of ischaemic heart disease are attributable to hypertension.

In our recent genome-wide association study using an extreme case-control design, we discovered a SNP (rs13333226 at position 16:20365654) in the 5’ region of the Uromodulin gene (UMOD), also known as Tamm-Horsfall glycoprotein (THP) to be associated with hypertension. The minor G allele of rs13333226 was associated with lower risk of hypertension, decreased urinary uromodulin excretion, and higher glomerular filtration rate. Furthermore, the association with hypertension was shown to be independent of renal function indicating a possible pleiotropic effect, as SNPs highly correlated with rs13333226 were shown to be associated with kidney function in independent GWAS studies. The genotype association of rs13333226 and urinary UMOD excretion was more pronounced with low salt intake, and blunted with high salt intake, indicating a possible gene-environment interaction.

We have extended these findings with work in UMOD KO mice which show a lower baseline blood pressure and are not sensitive to salt induced changes in blood pressure. Our data indicate that UMOD has a role in BP regulation and may protect from salt induced increase in BP. UMOD is selectively produced in the thick ascending limb of the loop of Henle in the kidney. and exists predominantly as a polymer in luminal fluid.

Proposal Plan: Molecular characterisation of human and mouse uromodulin transcripts and binding partners.

In this project, we will utilise RNA from a large panel of human kidneys (~100) grouped according to hypertension status, as well as the UMOD knock out mouse. We have access to human and rodent RNAseq data that we will analyse using different strategies including biological pathways using gene set enrichment and Ingenuity Pathway Analysis. We are also interested in identifying binding partners of UMOD under different environmental stressors and assessing potential transcription factor binding in the promoter region using Electrophoretic Mobility shift Assays (EMSA).

Project aims

  • Assess humanUMOD transcripts using RNAseq  Explore biological pathways using Ingenuity Pathway Analysis. 
  • ValidateRNAseq gene expression changes using our panel of human kidneys prioritised by pathway analysis. 
  • Use immunoprecipitation and mass spectrometry to identify binding partners of UMOD in human renal tissueto characterise potential mechanisms of action in disease.
  • Assess the genetic contribution of UMOD in large scale data including UK Biobank

 

Techniques used: 

  • Isolation ofDNA and RNA 
  • qRT-PCR and Sanger sequencing
  • PCRand cloning 
  • Western analysis
  • AnalysingRNAseq transcript data and other ‘Omic’ platforms
  • Biological pathway and data integration analysis
  • Electrophoretic Mobility ShiftAssays to identify potential binding partners of uromodulin and assess potential binding of predicted transcription factors using mass spectrometry. 

References:

  1. Small HY, Morgan H, Beattie E, Griffin S, Indahl M, Delles C, Graham D. Abnormal uterine artery remodelling in the stroke prone spontaneously hypertensive rat. Placenta. 2016 Jan;37:34-44.
  2. Morgan HL, Butler E, Ritchie S, Herse F, Dechend R, Beattie E, McBride MW, Graham D. Modeling Superimposed Preeclampsia Using Ang II (Angiotensin II) Infusion in Pregnant Stroke-Prone Spontaneously Hypertensive Rats. Hypertension. 2018 Jul;72(1):208-218.
  3. Scott K, Morgan HL, Delles C, Fisher S, Graham D, McBride MW. Distinct uterine artery gene expression profiles during early gestation in the stroke-prone spontaneously hypertensive rat. Physiological Genomics, 15 Mar 2021, 53(4):160-17

---

+++

Deciphering disease mechanisms underlying hypertensive pregnancy

Supervisors: Delyth GrahamMartin McBride

Project outline: The incidence of cardiovascular disease amongst women of child-bearing age is increasing. Consequently there is a greater prevalence of hypertensive disorders in pregnancy, in particular pre-eclampsia (PE), which is a leading cause of maternal and foetal morbidity and mortality. Despite its increased prevalence, the mechanisms underlying key pathological features of the disease remain unclear, and there are currently no effective clinical interventions.

The stroke prone spontaneously hypertensive rat (SHRSP) is an established model of human cardiovascular disease, which exhibits chronic hypertension during pregnancy1. This model can be progressed to the more severe pregnancy complication, superimposed PE, through angiotensin II administration mid-gestation2. Our recent studies in this model have identified pregnancy- and disease- dependent alterations in the uterine artery transcriptome relative to the normotensive control strain3. 

In this project, the specific molecules and pathways identified in our previous SHRSP studies will be explored mechanistically to determine their role in the pathogenesis of hypertensive pregnancy in order to identify new targets of therapeutic or diagnostic interest.

Techniques used: The student will receive training in a wide range of techniques, including animal models of hypertension and PE, cell culture, imaging, molecular biology approaches as well as RNASeq and other ‘Omics’ datsets and bioinformatic and pathway analysis. This PhD project will provide opportunities to develop an almost unique combination of in vivo, in vitro and molecular skills set.

References:

  1. Small HY, Morgan H, Beattie E, Griffin S, Indahl M, Delles C, Graham D. Abnormal uterine artery remodelling in the stroke prone spontaneously hypertensive rat. Placenta. 2016 Jan;37:34-44.
  2. Morgan HL, Butler E, Ritchie S, Herse F, Dechend R, Beattie E, McBride MW, Graham D. Modeling Superimposed Preeclampsia Using Ang II (Angiotensin II) Infusion in Pregnant Stroke-Prone Spontaneously Hypertensive Rats. Hypertension. 2018 Jul;72(1):208-218.
  3. Scott K, Morgan HL, Delles C, Fisher S, Graham D, McBride MW. Distinct uterine artery gene expression profiles during early gestation in the stroke-prone spontaneously hypertensive rat. Physiological Genomics, 15 Mar 2021, 53(4):160-17

---

+++

Investigating the role of endoplasmic reticulum stress as mechanisms of disease

SupervisorsTom Van Agtmael and Christian Delles

Vascular diseases are a major health problem for which there is an urgent need for treatments. Increasing our understanding of the underlying molecular disease mechanisms will aid in the development treatment strategies.

We have previously identified that mutations in the genes Col4a1 and Col4a2 cause a rare syndrome that leads to vascular, eye, kidney and muscle defects. These mutations cause defects to the extracellular matrix and a cell stress response called endoplasmic reticulum (ER) stress, caused by is also a feature of disease due to mutations in other secreted proteins, and major diseases in the general population including high blood pressure, heart failure, as well as eye and kidney defects leading to blindness and chronic kidney disease.However, the actual role of and mechanisms by which ER stress leads to many of these diseases remains unclear.

To address this gap in our knowledge, in this project you will employ novel mouse models that we generated to determine in vivo the role of ER stress in disease. Combined with cell culture models, imaging and proteomics/next generation sequencing you will investigate the molecular mechanisms by which ER stress affects the vasculature. In so doing, this project will increase our fundamental understanding of ER stress and may help the development of novel disease-mechanism based treatments for vascular disease such as stroke, and/or hypertension.

Techniques used: you will be trained in a large variety of techniques using animal models, cell culture, molecular and biochemical approaches, imaging, as well as RNASeq and proteomics etc.

---

+++

Investigating disease mechanisms of collagen IV disease including intracerebral haemorrhage

Supervisors: and Alyson Miller

15% of strokes are due to intracerebral haemorrhage (ICH), for which there is no treatment. and absence of specific effective treatments indicates increased knowledge of its pathomolecular basis is required. Recent genetic data has identified an important role for the protein collagen IV in stroke due to haemorrhage. Mutations in collagen IV also cause eye, kidney and muscle disease for there are also no treatments. We and others have showed the mutations and variants in collagen can cause defects to the extracellular matrix as well as a cell stress response called ER stress.

This project will use a powerful set of bespoke mouse models to determine in vivo the relative contribution of BM defects and ER stress to ICH as well as eye and kidney defects due to collagen IV. This will be combined with vascular physiology and molecular approaches, including transcriptomics and/or proteomics, to identify novel mechanisms.

Importantly, you will validate these mechanisms in patients. This project can be tailored to the interests of the candidate but will transform our knowledge of molecular mechanisms of stroke and disease due to collagen. This will aid development of precision medicine treatments.

Techniques used: you will be trained in a large variety of techniques crossing animal models of stroke, analysis of vascular function, molecular and biochemical approaches, imaging etc.

---

+++

Developing gene therapy approaches for stroke, eye and kidney disease due to mutations in collagen

Supervisors:  and Mark Bailey (SoLS)

Mutations in collagen IV cause a severe genetic disorder that includes brain bleeding, eye and kidney disease. In addition rare mutations also contribute to stroke in the general population. There are no treatments available for these disease, and the complex nature of the disease further hinders treatment development.

A gene therapy based approach is therefore an attractive solution to develop a potential cure for this disease.

Using a panel of cell lines from patients and endothelial cells with mutations, you will investigate different gene therapy approaches to silence the expression of collagen IV mutations. This would involve developing different strategies and introduce them into cell culture to determine if they can overcome the cell defects of these mutations. If successful this could be translated into treatments for our animal models of diseases due to collagen mutations.

Techniques used: You will use a large variety of molecular biology approaches for the design and cloning of gene therapy approaches, cell culture, analysis of endothelial cell function (eg. angiogenesis assays), biochemical and molecular analysis, imaging etc.

---

+++

Investigating the role of endoplasmic reticulum stress as mechanisms of cardiovascular disease

Supervisors: Tom Van Agtmael and Christian Delles

Vascular diseases including haemorrhagic stroke are a major health problem for which there is an urgent need for treatments. Increasing our understanding of the underlying molecular disease mechanisms will aid in the development treatment strategies.

We have previously identified that mutations in the genes Col4a1 and Col4a2 cause stroke and vascular disease. These mutations cause defects to the extracellular matrix and a cell stress response called endoplasmic reticulum (ER) stress, caused by misfolding of the mutant collagen protein. Interestingly ER stress has also been observed in other vascular diseases in the general population including high blood pressure and heart failure. However, the actual role of ER stress to these diseases including Col4a1 disease remains unclear.

To address this gap in our knowledge, in this project you will employ novel mouse models that we generated to determine in vivo the role of ER stress in disease. Combined with cell culture models, imaging and proteomics/next generation sequencing you will investigate the molecular mechanisms by which ER stress affects the vasculature. In so doing, this project will increase our fundamental understanding of ER stress and may help the development of novel disease-mechanism based treatments for vascular disease such as stroke, and/or hypertension.

Techniques used: you will be trained in a large variety of techniques using animal models, cell culture, molecular and biochemical approaches, imaging, as well as RNASeq and proteomics etc.

---

+++

Runx1 and Heart Failure

Supervisor: Dr C Loughrey, Dr S NicklinEwan Cameron

Research area: Heart research

Project outline: Coronary heart disease (CHD) leading to myocardial ischaemia is the predominant cause of heart failure (HF) and premature mortality in the UK. CHD occurs when the blood vessels of the heart (coronary arteries) become narrowed by fatty material (atheroma) and reduce blood flow to heart muscle (myocardial ischaemia). If the coronary artery is occluded then an area of lethal tissue injury in heart muscle called a myocardial infarction (MI) can be produced. The subsequent structural and functional changes in the surviving heart muscle can lead to poor cardiac pump function and HF. Novel therapeutic strategies to preserve cardiac pump function are urgently needed to treat patients with myocardial infarction and thereby improve patient survival rates and quality of life.

The Runx family of genes (Runx1,2&3) encode for DNA binding transcription factors (Runx1,2&3) which regulate gene expression. Recently, increased Runx1 expression has been demonstrated in the hearts of patients with MI. In line with these data, our recent work demonstrates increased Runx1 expression in a mouse model of MI.

However, despite these observations, the role Runx1 plays in heart function remains unknown. We have made a novel and exciting discovery that higher Runx1 expression levels correlate with poor cardiac pump function. In order to corroborate this finding, we have produced a heart-specific knockout of Runx1. When MI is induced in this transgenic model, cardiac pump function is markedly improved suggesting that reducing Runx1 expression in the heart is a novel therapeutic approach to limit the progression of cardiac dysfunction in patients with MI.

Project aims: This studentship will investigate the relationship between Runx1 expression in the heart and the development of heart failure. In addition, the project will develop therapeutic strategies to reduce Runx1 expression in cardiac disease in order to prevent progression to heart failure.

Techniques used: The project will enable the student to be trained in in vivo rodent models of heart disease, integrative physiology, molecular biology and gene therapy approaches.

References:

Contact email: christohper.loughrey@glasgow.ac.uk

---

+++

Assessing therapeutic strategies to target the counter-regulatory renin-angiotensin system in cardiovascular disease

Supervisors: Dr Stuart Nicklin (with Dr Christopher Loughrey, Dr Lorraine Work)

Research area: Institute of Cardiovascular & Medical Sciences

Project outline: The renin angiotensin system (RAS) is a hormonal cascade mediating cardiovascular function. The RAS is key to the development of cardiovascular diseases, including cardiac remodelling in hypertension and heart failure and atherosclerosis. A counter-regulatory RAS exists, centred on the angiotensin converting enzyme (ACE) homologue ACE2 and angiotensin 1-7 [Ang-(1-7)], highlighting additional key mediators of the RAS which may be therapeutic targets in cardiovascular disease.

We have also discovered that Ang-(1-9), a metabolite of the Angiotensin II precursor angiotensin I, is a RAS hormone. We have demonstrated that Ang-(1-9) is able to antagonise the pathophysiological effects of AngII in cardiomyocytes, fibroblasts and vascular smooth muscle cells via the angiotensin type 2 receptor.

We are now investigating therapeutic approaches for peptides and enzymes of the counter-regulatory axis of the renin angiotensin system using adenoviral and adeno-associated viral gene transfer vectors and extracellular vesicles as delivery vehicles in cardiovascular disease models including hypertensive cardiomyopathy, myocardial infarction and acute vascular injury.

Project aims: To develop and assess molecular therapeutic approaches to deliver counter-regulatory renin angiotensin system components in cardiovascular disease.
Techniques used: Cell culture in both primary cells and cell lines and in vivo models of cardiovascular disease, molecular biology techniques, construction and testing of replication deficient viral gene transfer vectors, isolation and characterisation of extracellular vesicles.

Techniques used: Cell culture in both primary cells and cell lines and in vivo models of cardiovascular disease, molecular biology techniques, construction and testing of replication deficient viral gene transfer vectors, isolation and characterisation of extracellular vesicles.

References:

  • C Fattah, K Nather, CS McCarroll, M Hortigon, V Zamora Rodriguez, M Flores-Munoz, L McArthur, L Zentilin, M Giacca, RM Touyz, GL Smith, C Loughrey, SA Nicklin. Gene therapy with angiotensin-(1-9) preserves left ventricular systolic function post-myocardial infarction via a direct inotropic effect. (2016). THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 68: 2652-2666.
  • C McKinney, C Fattah, C Loughrey, SA Nicklin. (2014). Cardiac and vascular remodelling: effects of the counter-regulatory renin angiotensin system peptides, Ang-(1-7) and Ang-(1-9). CLINICAL SCIENCE, 126: 815-827.
  • M Flores-Muñoz, LM Work, K Douglas, L Denby, AF Dominiczak, D Graham, SA Nicklin. (2012). Angiotensin-(1-9) attenuates cardiac fibrosis in the SHRSP via the angiotensin type 2 receptor. HYPERTENSION, 59(2):300-307.
  • A Pashova, LM Work and SA Nicklin. (2020). The role of extracellular vesicles in neointima formation post vascular injury. CELLULAR SIGNALLING, 18;76:109783. doi: 10.1016/j.cellsig.2020.109783.
  • McFall A, Nicklin SA, Work LM. The counter regulatory axis of the renin angiotensin system in ischaemic stroke: insight from preclinical studies and potential as a therapeutic target. CELLULAR SIGNALLING, 2020 Dec;76:109809. doi: 10.1016/j.cellsig.2020.109809. Epub 2020 Oct 13.

Contact address and email:

Professor Stuart A Nicklin BSc (Hons) PhD
Professor of Cardiovascular Molecular Therapy
Institute of Cardiovascular and Medical Sciences
College of Medical, Veterinary and Life Sciences
University of Glasgow
126 University Place
Glasgow G12 8TA
Email: stuart.nicklin@glasgow.ac.uk
Tel: +44 (0)141-330-2521

---

+++

Developing Therapeutic approaches for haemorrhagic stroke

Supervisor: Dr. Tom Van Agtmael

Research area: Mouse genetics, haemorrhagic stroke, molecular cell biology, extracellular matrix, vascular disease, collagen, endoplasmic reticulum stress

Project outline: Stroke costs UK Society ~£8 billion annually with haemorrhagic stroke accounting for 15% of adult and 50% of paediatric stroke. There are no treatment available for haemorrhagic stroke, in part due to a poor understanding of the underlying molecular cause.
Collagen IV is the major component of a type of extracellular matrix called the basement membrane that provides essential structural support to blood vessels. We and others have shown that mutations in COL4A1 or COL4A2 (encoding collagen IV proteins) cause familial and sporadic haemorrhagic, indicating these mutations may be more common than previously expected and a potential contribution to stroke in the general population (1). Our results also reveal that endoplasmic reticulum (ER)-stress due to intracellular accumulation of mutant collagen IV is associated with disease development, and that treatment of collagen IV mutant cells can reduce ER-stress (2). This provides a golden opportunity to identify the disease causing mechanisms and explore therapeutic approaches for collagen IV diseases including haemorrhagic stroke.
We have brought together a unique cohort of cell lines from patients and animal models with Col4a1 mutations to investigate the disease mechanisms of these mutations and determine how cells respond to these mutations. The identified pathways will then be modified in cell line and animal models to investigate their role in disease development and identify their potential as a therapeutic target. As FDA approved compounds are available, this will directly inform on and may identify therapeutic approaches for haemorrhagic stroke.

Project aims:

  • Exploring genetic and high throughput approaches to identify pathways that influence disease development
  • Identify the ability of small compounds to prevent the pathological effects of collagen IV mutation in cells.
  • Modification of disease development in animal models

Techniques used: State of the art imaging techniques including 3-dimensional electron microscopy, confocal microscopy and atomic force microscopy. Molecular cell biology, animal models, MRI imaging, transcriptomics.

References:

  • Plaisier E, et al. Role of COL4A1 Mutations in the Hereditary Angiopathy with Nephropathy, Aneurysm and Cramps (HANAC) Syndrome. New Eng J Med 2007, 357, 2687-2695
  • Murray LS et al. Chemical chaperone treatment reduces intracellular accumulation of mutant collagen IV and ameliorates the cellular phenotype of a COL4A2 mutation that causes haemorrhagic stroke. Hum Mol Genet 2014, 23:283-92

Contact address and email:

tom.vanagtmael@glasgow.ac.uk
Dr. Tom Van Agtmael
Institute of Cardiovascular & Medical Sciences
College of Medical, Veterinary and Life Sciences
Davidson Building
University of Glasgow
University Avenue
Glasgow, G12 8QQ
United Kingdom
Phone: +44 (0)141 330 6200

---

Overview

The Institute of Cardiovascular & Medical Sciences (ICAMS) is a successful and vibrant research institute with outstanding training and learning opportunities. Our purpose-built British Heart Foundation (BHF) Cardiovascular Research Centre houses state-of-the-art laboratories and facilities and we are one of only six BHF Centres of Excellence in the UK.

Our research strengths have been integrated into substantial, well-resourced thematic programmes that build on the strengths of individual, clinical and non-clinical principal investigators. Working in basic, translational and clinical research, our strength is in elucidating mechanisms of cardiovascular disease, identifying biomarkers of disease, identifying therapeutic targets and developing and designing novel therapeutic strategies that will lead to clinical trials.

Individual research projects are tailored around the expertise of principal investigators within the institute. Basic and clinical projects are available for study. A variety of approaches are used, including molecular biology, biochemistry, epidemiology, mathematical modelling, bioinformatics, genetics, cell biology (including advanced in vitro and in vivo imaging), immunology and polyomics (genomics, transcriptomics, proteomics, metabolomics etc).

Specific areas of interest include:

  • vascular science and medicine
  • cardiovascular biology and cell signalling
  • cardiovascular gene therapy for the treatment of vascular disease
  • basic and clinical cerebrovascular disease e.g. stroke 
  • stem cell therapies for cerebrovascular disease
  • genetics, genomics and systems medicine 
  • adrenal corticosteroids in cardiovascular disease
  • diabetes, obesity, metabolic and renal disease
  • cardiovascular imaging
  • cardiovascular clinical trials
  • sport & exercise science & medicine

Study options

PhD

  • Duration: 3/4 years full-time; 5 years part-time

Individual research projects are tailored around the expertise of principal investigators.

MSc (Research)

  • Duration: 1 year full-time; 2 years part-time

MD (Doctor of Medicine)

  • Duration: 2 years full-time; 4 years part-time (for medically-qualified graduates only)

Entry requirements

A 2.1 Honours degree or equivalent.

English language requirements

Subject to confirmation for 2022 entry

For applicants whose first language is not English, the University sets a minimum English Language proficiency level.

International English Language Testing System (IELTS) Academic module (not General Training)

  • 6.5 with no sub-test under 6.0. 
  • Tests must have been taken within 4 years 5 months of start date. Combined scores from two tests taken within 6 months of each other can be considered.

Common equivalent English language qualifications

All stated English tests are acceptable for admission to this programme:

TOEFL (ib, my best or athome)

  • 90 with minimum R 20, L 19, S 19, W 23. 
  • Tests must have been taken within 4 years 5 months of start date. Combined scores from two tests taken within 6 months of each other can be considered.

PTE (Academic)

  • 60 with minimum 59 in all sub-tests.
  • Tests must have been taken within 4 years 5 months of start date. Combined scores from two tests taken within 6 months of each other can be considered.

Glasgow International College English Language (and other foundation providers)

  • 65%.
  • Tests are accepted for academic year following sitting.

University of Glasgow Pre-sessional courses

  • Tests are accepted for academic year following sitting.

Alternatives to English Language qualification

  • Undergraduate degree from English speaking country (including Canada if taught in English)
  • Undergraduate 2+2 degree from English speaking country
  • Undergraduate 2+2 TNE degree taught in English in non-English speaking country
  • Masters degree from English speaking country
  • Masters degree (equivalent on NARIC to UK masters degree) taught in English in non-English speaking country.

For international students, the Home Office has confirmed that the University can choose to use these tests to make its own assessment of English language ability for visa applications to degree level programmes. The University is also able to accept an IELTS test (Academic module) from any of the 1000 IELTS test centres from around the world and we do not require a specific UKVI IELTS test for degree level programmes. We therefore still accept any of the English tests listed for admission to this programme.

Pre-sessional courses

The University of Glasgow accepts evidence of the required language level from the English for Academic Study Unit Pre-sessional courses. We also consider other BALEAP accredited pre-sessional courses:

Fees and funding

Fees

2022/23

  • UK: £4596
  • International & EU: £23,950

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

Alumni discount

We offer a 20% discount to our alumni on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed Junior Year Abroad, Exchange programme or International Summer School with us. The discount is applied at registration for students who are not in receipt of another discount or scholarship funded by the University. No additional application is required.

Funding for EU students

The Scottish Government has confirmed that fees for EU students commencing their studies 2020/21 will be at the same level as those for UK student. 

From 2021/22, new entrant EU students will pay the same fees as all other international students.

Possible additional fees

  • Re-submission by a research student £540
  • Submission for a higher degree by published work £1,355
  • Submission of thesis after deadline lapsed £350
  • Submission by staff in receipt of staff scholarship £790

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

+++

2021/22 fees

  • UK: £4,500
  • International & EU: £23,000

Additional fees for all students:

  • Re-submission by a research student £540
  • Submission for a higher degree by published work £1,355
  • Submission of thesis after deadline lapsed £350
  • Submission by staff in receipt of staff scholarship £790

---

Funding

The iPhD  is not supported by University of Glasgow Scholarship/Funding

Support

Resources

Our laboratories are well resourced and we offer a wide range of cutting-edge research facilities, including core facilities in:

  • optical imaging
  • electrophysiology
  • magnetic resonance imaging
  • spectroscopy
  • cell biology
  • high throughput genotyping
  • phenotyping
  • clinical trials
  • a wide range of cellular, molecular and biochemical analysis tools

Our excellent facilities underpin a bench to bedside approach that will equip you with research specific and generic training and skills complementary to a wide range of career options. We can tailor your study pathway to the precise aspects of cardiovascular research that suit your objectives.

You will emerge equipped with the skills necessary for a career in the highly competitive field of cardiovascular science and medicine. Future career opportunities include basic and clinical cardiovascular research in academia or industry, education, NHS, clinical biochemistry, public health bodies, media and publishing, funding agencies and scientific charities.

Graduate School

The College of Medical, Veterinary & Life Sciences Graduate School provides a vibrant, supportive and stimulating environment for all our postgraduate students. We aim to provide excellent support for our postgraduates through dedicated postgraduate convenors, highly trained supervisors and pastoral support for each student.
 
Our overarching aim is to provide a research training environment that includes:

  • provision of excellent facilities and cutting edge techniques
  • training in essential research and generic skills
  • excellence in supervision and mentoring
  • interactive discussion groups and seminars
  • an atmosphere that fosters critical cultural policy and research analysis
  • synergy between research groups and areas
  • extensive multidisciplinary and collaborative research
  • extensive external collaborations both within and beyond the UK 
  • a robust generic skills programme including opportunities in social and commercial training

How to apply

Identify potential supervisors

All Postgraduate Research Students are allocated a supervisor* who will act as the main source of academic support and research mentoring. You may want to identify a potential supervisor and contact them to discuss your research proposal before you apply. Please note, even if you have spoken to an academic staff member about your proposal you still need to submit an online application form.

You can find relevant academic staff members with our staff research interests search.

*iPhD applicants do not need to contact a supervisor, as you will start your programme by choosing a masters from our Taught degree programmes A-Z [do not apply directly to a masters].

Gather your documents

Before applying please make sure you gather the following supporting documentation:

  1. Final or current degree transcripts including grades (and an official translation, if needed) – scanned copy in colour of the original document.
  2. Degree certificates (and an official translation, if needed): scanned copy in colour of the original document
  3. Two references on headed paper and signed by the referee. One must be academic, the other can be academic or professional [except iPhD applicants, where only one academic or professional reference is required]. References may be uploaded as part of the application form or you may enter your referees contact details on the application form. We will then email your referee and notify you when we receive the reference.  We can also accept confidential references direct to rio-researchadmissions@glasgow.ac.uk, from the referee’s university or business email account.
  4. Research proposal, CV, samples of written work as per requirements for each subject area. iPhD applicants do not need to submit any of these as you will start your programme by choosing a masters.

Notes for iPhD applicants

  • add 'I wish to study the MSc in (chosen subject) as the masters taught component of the iPhD' in the research proposal box
  • write 'n/a' for the supervisor name
Apply now

I've applied. What next?

If you have any other trouble accessing Applicant Self-Service, please see Application Troubleshooting/FAQs. 

Contact us

Before you apply

PhD/MSc/MD: email mvls-gradschool@glasgow.ac.uk

iPhD: email mvls-iphd@glasgow.ac.uk

After you have submitted your application

PhD/MSc/MD/iPhD: contact our Admissions team

Any references may be submitted by email to: rio-researchadmissions@glasgow.ac.uk