Job Description

About ARU:

We are ranked in the world\xe2\x80\x99s top 350 institutions in the 2022 Times Higher Education World University Rankings, and we are a global university transforming lives through innovative, inclusive and entrepreneurial education and research. Our research institutes and four faculties bridge scientific, technical and creative fields. We deliver impactful research which tackles pressing issues and makes a real difference to our communities. Our academic excellence has been recognised by the UK\xe2\x80\x99s Higher Education funding bodies, with 16 of our research areas assessed as world-leading. In 2021, we were awarded the Queen\xe2\x80\x99s Anniversary Prize for our world-leading music therapy work.

About the Role:

Anglia Ruskin University is inviting applications for a fully-funded Vice-Chancellor\xe2\x80\x99s PhD Scholarship for a period of 36 months within the School of Allied Health and Social Care, Faculty of Health and Medical Sciences.

Project Description:

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.

Fibrosis is the result of dysregulated wound healing, where functional tissue is replaced 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 driven by a key cell type called fibroblasts, which upon injury, transform into myofibroblasts. During wound healing and fibrosis myofibroblasts are responsible for the excessive production of extracellular matrix.

Extracellular vesicles (EVs) are small particles released by cells and have gained attention in fibrosis research as they can carry molecules that influence fibrosis development. Some EVs activate fibroblasts and promote excessive extracellular matrix production, contributing to fibrosis. Others play roles in inflammation and tissue repair.

We have recently discovered that EVs derived from Peyronie\xe2\x80\x99s disease-derived myofibroblasts can prevent myofibroblast transformation in vitro. Specifically, we have identified the multifunctional protein TSG-6 (Tumour Necrosis Factor-\xce\xb1-Stimulated Gene-6) as a key mediator of this effect. Our discovery marks the first instance in which myofibroblast-derived EVs have been implicated in exerting an anti-fibrotic effect through TSG-6.

This project seeks to provide compelling evidence of TSG-6\'s pivotal role in promoting fibrosis resolution and may pave the way for innovative anti-fibrotic treatments. To accomplish these objectives, we propose an integrative approach that combines genomic, transcriptomic, proteomic and secretomic analyses. Additionally, we intend to apply genetic modification techniques to fibroblasts and myofibroblasts obtained from patients affected by various fibrotic conditions. This project represents a pioneering effort in the field of fibrosis research, as it marks the first comprehensive analysis that integrates these cutting-edge techniques on such a scale.

The award is subject to the successful candidate meeting the studentship Terms and Conditions which can be found on our website alongside further information about the project: and enquiries can be directed to

We are committed to safeguarding and promoting welfare of our staff and students and expect all staff to share this commitment.

We value diversity at ARU and welcome applications from all sections of the community.

Anglia Ruskin University