The emphasis of our work is the cellular response to metabolic stress, particularly in relation to cancer, chronic metabolic disease, and the interaction between the foeto-placental unit and maternal obesity in pregnancy.
Hormonal action requires the transfer of information from the extracellular environment into cells, where downstream target processes (in the nuclear and extra-nuclear compartments) are affected.
Research within the Division of Metabolic and Vascular Health is aimed at understanding the mechanisms through which such ‘signal transduction’ occurs normally, or is disrupted under different (patho)physiological conditions.
Current research in this field includes:
- The role of splice variants of Corticotrophin Releasing Hormone (CRH) receptors in the modulation of placental function and oestrogen-responsiveness of breast cancer cells
- The integration of inflammatory and adipocyte differentiation responses in obesity by Fyn Kinase
- The role of Nrf2 in cellular stress responses to environmental toxins, oxidative stress, chronic metabolic dysfunction and inflammation, with particular emphasis on the effects of ageing, diabetes and renal failure
- Elucidation of the signalling pathways involved in the regulation of water balance in the hypothalamus, and their disruption in diabetes insipidus
- MAPKinase signalling pathways involved in the regulation of glucose uptake by muscle cells
- The effects of altered interactions between glucose and fatty acid metabolism, and cellular signalling pathways regulating cellular proliferation, on cancer development and progression
- The effects of adipokines and other cytokines on adipose tissue and cardiac cellular responses to stress
Our research addresses the following issues:
- The responses of breast cancer cells and the placenta to modulation of cellular signalling pathways affected by components of the hypothalamic-pituitary-adrenal axis
- The effects of ageing, diabetes and end-stage kidney disease on cellular responses to stress
- Prevention of cardiac damage due to ischaemia reperfusion of the heart
- Improvement of the regulation of anti-diuretic hormone secretion in diabetes insipidus
- Dissociation of the chronic sub-clinical inflammation and obesity
We receive funding from the following sources:
- Medical and Life Sciences Research Fund
- Coventry Health Charities
- Philantropic donations
- Technology Strategy Board
- EU FP7 Collaborative Projects
