The interview for this project is expected to take place on Thursday 27 April.
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 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, you'll 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).
You'll be working as part of the Fibrosis Research Group at our Chelmsford campus. This project will use state-of-the-art cell and molecular techniques based at ARU in collaboration with Intelligent Omics and Nottingham Trent University.
Ideally, you'll have a background in bioinformatics and/or cell biology.
If you would like to discuss this research project please contact Dr Marcus Ilg: [email protected]Apply online by 19 March 2023
This successful applicant for this project will receive a Vice Chancellor’s PhD Scholarship which covers Home tuition fees and provides a UKRI equivalent minimum annual stipend for three years. For 2022/3 this was £17,688 per year. The award is subject to the successful candidate meeting the scholarship terms and conditions. Please note that the University asserts the right to claim any intellectual property generated by research it funds.