Research

Characterising novel mechanisms of cardiovascular calcification.

Dr Vicky MacRae's lab has elucidated a range of novel mechanisms underpinning the calcification process, which may pave the way for future therapeutic strategies against cardiovascular calcification. Her research has investigated the role of growth factors (e.g. BMP9), steroids (e.g. glucocorticoids, testosterone) and metabolic pathways (e.g. glycolysis, purinergic signalling and autophagy). During these studies, she has collaborated extensively with clinicians from Edinburgh, Europe and the USA to translate her findings to human tissues. Throughout her independent research career, she has particularly focused on the biology of ectonucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1), which plays a critical role in the rare disease Generalised Arterial Calcification of Infancy (GACI).

Elucidating pathways underpinning bone formation. 

Dr Vicky MacRae's lab has shown a crucial local role for osteoblast ENPP in skeletal development and a secondary metabolic impact that predominantly maintains insulin sensitivity. This work, underpinned by international collaborations (Columbia, Hawaii, Montreal, San Diego) has advanced the field’s understanding of a novel bone/energy axis.  

A series of collaborative PhD studentship projects led by Professor Colin Farquharson (The Roslin Institute, University of Edinburgh) have established novel roles for PHOSPHO1 during the (i) anabolic bone response to parathyroid hormone delivery, (ii) regulation of insulin resistance and (iii) mediation of bone mineral density in renal osteodystrophy.

Investigating mechanisms of mitral valve disease.

This collaborative research programme, led by Professor Brendan Corcoran (University of Edinburgh) has directly advanced the veterinary cardiovascular field through the development of new canine cell culture models and has attracted support from industry (Pfizer Animal Health) and charity (Dog’s Trust) sources. Our studies have identified a novel role for TGFβ signalling in canine myxomatous mitral valve disease (CMVD), through the modulation of senescence. This work further highlighted senolytics as a potential therapeutic strategy against CMVD, the most common cardiovascular disease in dogs.