Exploring mechanisms and novel treatment strategies for age-associated cardiovascular disease

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Preliminary findings from our laboratory suggest that MFGE8 is associated with the partial dedifferentiation of VSMCs from a contractile phenotype. MFGE8 overexpression in the presence of calcifying conditions appears to exacerbate aortic calcification. This highlights the potential for MFGE8 mediated signalling as a novel therapeutic target for vascular calcification with ageing. It is hypothesised that the age-dependent increases in MFGE8 expression is capable of promoting calcification and medin aggregation. Aims: 1. To assess whether MFGE8 promotes the incidence of vascular calcification 2. To investigate whether MFGE8 and calcification induce alterations to vascular physiology 3. To determine the signalling pathway associated with MFGE8 mediated responses in the vasculature 4. To elucidate how medin is cleaved from MFGE8