My research is interdisciplinary and sits at the interface between the basic sciences and medicine. Research in my laboratory is focused upon how metal ions are handled in the body and the roles they play in regulating medically/physiologically relevant processes. Collectively, my work provides detailed and reliable data relating to the transport and speciation of metal ions (particularly zinc and calcium) in the circulation and new insights into their cellular functions and role in disease states. Currently my team are examining ways in which defective metal handling contributes to pathogenesis of cardiovascular diseases, including vascular eye disease and dementia.

Our work currently spans three main areas:

1. Zinc, Fatty Acids, and Thrombotic Risk in Diabetes
   Type 2 diabetes (T2D) affects nearly half a billion people globally, with cardiovascular disease, a leading cause of death in T2D. A key contributor is an enhanced thrombotic environment, driven by abnormal interactions between platelets and coagulation proteins. We have identified a novel mechanism in which elevated non-esterified fatty acids (NEFAs)—common in diabetes—disrupt zinc (Zn²⁺) binding to albumin, increasing free Zn²⁺ availability. This promotes Zn²⁺-dependent changes in fibrin clot structure and platelet function. Our work funded by the British Heart Foundation, is investigating how Zn²⁺ directly modulates fibrin network formation and its interactions with platelets and haemostatic molecules, providing new insight into thrombosis risk in diabetes.
2. Magnesium and Fibrinolysis in Type 1 Diabetes
   Vascular complications and increased thrombotic risk are major concerns in type 1 diabetes (T1D). We have identified lower plasma magnesium levels in individuals with T1D compared to controls, with this deficiency linked to hypofibrinolysis—a predictor of cardiovascular outcomes. We hypothesise that adequate magnesium is critical for normal haemostasis and are exploring how magnesium regulates fibrinolysis, whether supplementation improves thrombotic profiles and patient outcomes, and whether it causes structural changes in fibrinogen or plasminogen. Funded by Diabetes UK, our goal is to evaluate magnesium supplementation as a safe, cost-effective strategy to reduce cardiovascular risk in T1D.
3. Quantitative Proteomics and Metal-Protein Interactions
   In collaboration with Dr. Sally Shirran, we’ve established SWATH-MS proteomics to quantify hundreds of plasma proteins from minimal samples. This has enabled discovery of potential markers in macular degeneration and immune cell differentiation. We are now applying this to cancer diagnostics and to understand haemostatic changes triggered by metabolic disease states. We are also developing "speciomic" approaches to explore metal-protein interactions.

BSc(Hons) Biochemistry, University of Edinburgh; PhD, University of Edinburgh

Cancer; Cardiovascular disease; Metabolism; Metal-protein interactions; Metallomics; Plasma proteins; Proteomics