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Selective targeting of proteases for the treatment of chronic airways disease.


School of Pharmacy

Prof L Martin Applications accepted all year round Self-Funded PhD Students Only

About the Project

Cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) are both progressive airways diseases associated with cycles of infection and inflammation, lung tissue destruction and pulmonary decline. Intensive management needs and frequency in hospitalization give rise to significant treatment costs (UK £4.7 bn & USA $42.6 bn pa). New therapies targeting some of the specific cellular processes associated with these diseases could help improve both lung function and quality of life which would also reduce hospital admissions.
Lung damage is associated with impaired clearance mechanisms due to disease-specific triggers of airways dehydration. In normal airways, the epithelial sodium channel (ENaC) is predominantly silent however a protease-antiprotease imbalance present in chronic lung disease can cause a dysregulation of ENaC leading to increased Na+ absorption, airways dehydration, thickened mucus and impaired mucociliary clearance (MCC). As restoration of normal airway clearance mechanisms would serve to reduce the risk/number of life-limiting cycles of infection and lung injury, inhibition of ENaC represents an attractive therapeutic strategy for repiratory medicine, independent of etiology of disease.

We have already shown, using primary human CF bronchial epithelial cells, that first-in-class, highly selective, sub-nanomolar inhibitors, some of which are currently being developed as drug candidates, are highly effective inhibitors of ENaC signaling leading to an increase in airway surface liquid. The objective of this study is to see if similar beneficial effects can be observed using primary human airway epithelial cells derived from COPD donors. This project will conduct further mechanistic studies on ENaC and airways hydration, but also aims to explore other potential therapeutic benefits to include impact on inflammation and airway remodeling (fibrogenesis) as well as suppression of signaling pathways which could potentially reduce the muco-secretory/obstructive phenotype associated with COPD. Importantly, these studies directly align to the strategic research interests of the Martin group, and a collaborative relationship with an industry partner and provide opportunity for the successful applicant to benefit from the significant expertise of the research group.

Funding Notes

Applicants should have a 1st or high 2.1 (>67%) honours degree (or equivalent) in a relevant subject. Relevant subjects include Biochemistry, Pharmaceutical Biotechnology, Molecular Biology, Physiology, Biological/Biomedical Sciences or a closely related discipline. Students who have a 2.2 honours degree and a Master’s degree may also be considered, but the School reserves the right to shortlist for interview only those applicants who have demonstrated high academic attainment to date

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