Biomedical Science PhD project opportunities

Find out more about self-funded PhD projects in areas of biomedical science.

We already have supervisors active and engaged in the research topic in our School of Life Sciences.

Funded opportunities

Fixed term contract for 3 years, commencing September 2025.

Bursary of £20,780 per annum and a full fee-waiver for tuition fees.

Closing date: 31 May 2025

Interview date: TBC June 2025

About Anglia Ruskin University:

Anglia Ruskin is a vibrant workplace and our university is recognised both nationally and internationally. We have ambitious plans for the future, and we are determined that our students and staff will realise their full potential. Our main campuses in the cities of Cambridge, Chelmsford, London and Peterborough have been transformed with major capital investment. With an annual turnover of over £200m, we are a major force for higher education and one of the largest universities in the East of England.

About the position:

The calcification of arteries is a significant risk factor in the development of heart attacks and stroke. Identifying new pathways and novel pharmacological targets that prevent this process could therefore reduce the risk of cardiovascular disease.

As described in a review from our laboratory (1), vascular smooth muscle cells (VSMCs) are the predominant cell type involved in arterial calcification, and can change into a bone-like phenotype when subjected to a calcified environment. This is evident in the expression of bone-like factors, including the master transcription factor runt-related transcription factor 2 (Runx2).

Metformin has been used in type 2 diabetes treatment for over 60 years and is currently the most common diabetes treatment worldwide. However, there is growing evidence that metformin’s positive health actions extend beyond its capacity to modulate glucose metabolism, including cardiovascular benefits. Indeed, our recent paper shows that metformin exerts protective effects against arterial calcification through autophagy (cellular recycling) and the subsequent autophagic degradation of Runx2 (2). We also show that this mechanism involves p62, an important regulator of autophagy. Interestingly, a recent model proposes that autophagic cargo proteins can be concentrated and segregated through the polyubiquitin chain-induced phase separation of p62, forming “p62 bodies”. These p62 bodies serve as essential platforms for autophagosome formation (3).

This PhD project will test the hypothesis that the mechanism through which p62 mediates metformin’s protective effect against arterial calcification is phase separation (Aim 1) and the formation of p62 bodies in order to store Runx2 (Aim 2). Furthermore, this project will seek to develop a novel targeted protein degradation therapeutic, mirroring the targeted degradation of Runx2 by metformin (Aim 3).

The student will be trained to tackle fundamental scientific questions in a vibrant atmosphere in three laboratories with complementary and wide-ranging expertise in calcification biology (Professor Vicky MacRae), vascular research (Professor Vicky MacRae, Professor Havovi Chichger) and protein self-assembly (Dr Janet Kumita). The student will be trained in our laboratories based at both Anglia Ruskin University Cambridge (School of Life Sciences) and University of Cambridge (Department of Pharmacology), using a multidisciplinary approach including molecular techniques, advanced imaging and protein engineering. The student will be encouraged to present work at UK and International scientific conferences. Past students of the supervisors’ have typically published at least 2 scientific papers during their studentships and have secured high profile post-doctoral or industry positions.

References:

  1. Zhu et al. Mechanisms and clinical consequences of vascular calcification. Front Endocrinol (Lausanne). 2012 6;3:95.
  2. Phadwal et al. Metformin protects against vascular calcification through the selective degradation of Runx2 by the p62 autophagy receptor. J Cell Physiol. 2022 237(11):4303-4316.
  3. Sun et al. Polyubiquitin chain-induced p62 phase separation drives autophagic cargo segregation. Cell Res. 2018 28(4):405-415.

About the Studentship:

A 3-year studentship is offered, intended to start in September 2025, providing a tax-free stipend of £20,780 per annum plus tuition fees.

Project location: Cambridge campus. Prospective candidates who would not be Cambridge-based are encouraged to contact the principal supervisor prior to application (contact details below).

Candidates for this PhD Studentship must demonstrate outstanding qualities and be motivated to complete a PhD within 3 years.

Qualifications:

Applicants should have a minimum of a 2.1 Honours degree in a relevant discipline. An IELTS (Academic) score of 6.5 minimum (or equivalent) is essential for candidates for whom English is not their first language.

In addition to satisfying basic entry criteria, the University will look closely at the qualities, skills, and background of each candidate and what they can bring to their chosen research project in order to ensure successful and timely completion.

How to apply:

To apply, please visit Biomedical Science PhD, click 'Apply online' and complete the application form for full-time study with a start date of September 2025. Please ensure the reference 'PhD Studentship: Harnessing protein degradation as a therapeutic strategy to reduce cardiovascular disease' is clearly stated on the application form, under the title ‘Outline of your proposed research’.

Within this section of the application form, applicants should include a 500-word outline of the skills that they would bring to this research project and detail any previous relevant experience.

Interested applicants should direct initial queries about the project to Professor Vicky MacRae via email: [email protected]. For enquiries regarding the process and eligibility please contact [email protected].

Interviews are scheduled to take place in June 2025.

We value diversity at Anglia Ruskin University and welcome applications from all sections of the community.

Closing Date 31 May 2025.

Non-funded opportunities

Research Group

Biomedical Research Group

Proposed supervisory team

Dr Grisha Pirianov

Prof David Leake (University of Reading)

Theme

Translational Biomedicine

Summary of the research project

Background: Macrophages play a critical role in homeostasis and diseases. They can change their phenotype to perform differential activities in different phases of inflammatory response.

Polarized macrophages are broadly classified into two groups:

  • classical activated M1 (pro-inflammatory)
  • alternative activated M2 (anti-inflammatory).

It has been demonstrated that M1/M2 switch plays critical role in inflammation which is dependent on various factors such as bioavailability of different subsets of monocytes and macrophages, sequential monocytes recruitment into the tissue in the process of inflammation or response to different conditions. Furthermore, the misbalance of M1/M2 switch can lead to chronic inflammatory diseases. Undoubtedly the generation of novel anti-inflammatory drugs regulating M1/M2 switch is an important step for pharmacological intervention of chronic inflammatory-based diseases. Unfortunately, the current drug screening strategies are not based on macrophage polarization. The development of a phenotypic macrophage high-throughput assay will provide a platform for screening of pro or anti-inflammatory properties of the candidate molecule (preclinical drug validation) or FDA approved drugs library and selected compound libraries with known anti-inflammatory activity (clinical drug validation).

Main goal and objectives: The main goal of the study is to develop and validate a novel phenotypic macrophage high-throughput cell-based assay for anti-inflammatory drug screening activity. The two main objectives are:

  • to develop a cell-based M0/M1/M2 phenotypic screen
  • to investigate the effect of novel small molecules (TLR4 antagonists) and selected compound libraries with known anti-inflammatory activity on M0/M1/M2 screen.

Methodology: Cell culture and cell-based essays, western blotting, ELISA approaches.

Collaborations: This project is based on academic and industrial collaborations with Reading University and Innaxon, UK respectively.

Outcomes: Results from this project will evaluate the potential of the phenotypic macrophage high-throughput assay for drug screening as well as provide important information about the effect of the candidate molecules on macrophage polarisation and will contribute to their preclinical/clinical validation. This will represent a finding of great public and commercial impact as currently there are no macrophage cell-based phenotypic assays for drug screening. The proposed project will have a commercial value and we plan to secure protection of the arising intellectual property.

Where you'll study

Cambridge

Funding

This project is self-funded.

Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.

Next steps

If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.

Research Group

Biomedical Research Group

Proposed supervisory team

Dr Grisha Pirianov

Dr Dannielle Green

Theme

Biomedicine and Environmental Pollution

Summary of the research project

Background: Plastic production has risen from 1.5 to 450 million tons annually since the 1950’s and is set to double by 2045. The total weight of plastic on Earth already exceeds the overall mass of all land and marine animals and plastic pollutants have altered Earth’s processes to an extent that exceeds the threshold under which humanity can survive in the future (i.e., surpassing the planetary boundary). Micro and nano plastics are the most abundant form of solid waste on Earth on average, humans are exposed to an estimated 39,000 to 121,000 particles per year via ingestion of contaminated food, beverages and drinking water via inhalation. The World Health Organization recently concluded that although NMP may pose a threat to human health, we need more evidence on their potential effects, especially concerning the lower size range (nano) of particles. In response to concerns about conventional plastics, demand for biodegradable bio-based plastics is increasing. Many of these plastics do not rapidly degrade in the natural environment and can persist as NMP and can have the same negative impacts as conventional plastics. The impacts of biodegradable NMP on human health has not been tested. Based on current knowledge on NMP toxicity and hazard there are substantial gaps and future research needs. Most of the studies are based on NMP without any characterisation of their physico-chemical properties (size, shape, charge etc.) which create difficulties in interpretation of their toxicological profile. Secondly, a high number of studies have employed very high concentrations of NMP which do not reflect on real environmental conditions. Although toxicological studies have shown that NMP exposure may lead to health risk there is a lack of evidence that this can negatively affect the immune system which is primary related to measurement of human health risks. Therefore, future research must be focused on biokinetics and proinflammatory and toxicological properties of environmentally relevant NMP with well characterised physico-chemical properties consistent with their environmental degradation.

Main goal: This project will investigate the proinflammatory and toxicological properties on NMP generated from conventional and future biodegradable plastics.

There are three main objectives:

  1. To develop THP-1 macrophage polarisation model as a biosensor for screening and comparison of proinflammatory and toxicological properties on NMP from different plastics.
  2. To screen the toxicological and proinflammatory effects of NMP from different plastics on the macrophage polarisation biosensor model.
  3. To investigate the mechanism of action of selected NMP candidates in relation to their toxicological and proinflammatory properties on the macrophage polarisation biosensor model.

Methodology: Cell culture and cell-based essays, western blotting, ELISA, Flow Cytometry and antibody array approaches.

Collaborations: This project is based on national and international academic collaborations with University of Milano-Bicocca and Reading University.

Outcomes: The results from this project will be used to consolidate international networking and national and international collaborations and to apply for EU Horizon (Micro- and nano-plastics in our environment: understanding exposures and impacts on human health) and will build on the success of the REF2027 Impact Case Study by Dr Green “Reducing the impacts of single use plastics”. This research also compared conventional and biodegradable plastics but on environmental compartments as opposed to human health.

Where you'll study

Cambridge

Funding

This project is self-funded.

Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.

Next steps

If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.