Fibrosis is the cause of 45% of mortality in the Western world and is defined as the excessive accumulation of extracellular matrix in response to injury. Treatment options are currently limited, with only two drugs available, both approved for the treatment of lung fibrosis. Ultimately, fibrosis replaces the functional tissue with non-functional extracellular matrix and whilst this is particularly fatal in the vital organs (e.g. the heart or lungs), fibrosis can affect any organ or system in the body.
Fibrosis is a result of dysregulated wound healing, which is driven by a key cell type called fibroblast. These cells undergo transformation to a cell type called myofibroblast upon injury. During wound healing and fibrosis myofibroblasts are responsible for the excessive production of extracellular matrix. Our previous work highlighted that fibroblasts isolated from various tissues, behaved differently when given the same drug treatment to stop myofibroblast transformation (Ilg et al., 2022; Lapthorn et al., 2022).
We believe this is due to a phenomenon called heterogeneity which plays a key a role in the development of different fibrotic disorders and their response to drug treatment.
One of the key objectives of this project will be to understand what drives this heterogeneity within fibrotic disorders. Understanding these mechanisms can have implications for diagnosis or treatment modalities and unveil new directions for therapeutics. The other key objective will be to identify pathways or targets that are shared across the various fibrotic tissues to find a ‘silver bullet’ to treat multiple or all types of fibrosis, instead of developing single drugs that target single diseases.
To achieve these objectives, the student will generate and compare transcriptomic and proteomic data from fibroblasts and myofibroblasts of patients with different types of fibrosis (Peyronie’s disease, lung fibrosis, cardiac fibrosis, intra-abdominal adhesions, and hypertrophic scars). The candidate will be working as part of the Fibrosis Research Group (https://aru.ac.uk/health-education-medicine-and-social-care/research/groups/fibrosis) at our Chelmsford campus. This project will use state-of-the-art cell and molecular techniques based at Anglia Ruskin University in collaboration with Intelligent Omics and Nottingham Trent University.
The ideal candidate will have a background in bioinformatics and/or cell biology.
If you would like to discuss this research project please contact Dr Marcus Ilg ([Email Address Removed])
Candidate requirements
Applications are invited from UK fee status only. Applicants should have (or expect to achieve) a minimum upper second class undergraduate degree (or equivalent) in a cognate discipline. A Master’s degree in a relevant subject is desirable.
Applicants must be prepared to study on a full-time basis, attending at our Chelmsford campus.
Application Procedures
Applications for a Vice Chancellor’s PhD Scholarship are made through the application portal on our website: https://aru.ac.uk/research/postgraduate-research/vc-phd-scholarships
We will review all applications after the submission deadline of 19th March. We will contact shortlisted applicants in the week commencing 3rd April. Interviews will be held between 17th April to 2nd May.
If you have any queries relating to the application process or the terms and conditions of the Scholarships, please email [Email Address Removed].
Documentation required
You will need the following documents available electronically to upload them to the application portal (we can accept files in pdf, jpeg or Word format):
- Certificates and transcripts from your Bachelor and Masters degrees, (if applicable)
- Your personal statement explaining your suitability for the project
- Passport and visa, or evidence of EU Settlement Scheme (if applicable)
- Curriculum Vitae
Please note the application form will ask you to upload a research proposal. You should upload your personal statement in this section, as proposals are not required for this scholarship.
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