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

我们实验室的初步研究结果表明，MFGE8与VSMCs从收缩表型部分去分化有关。在钙化情况下，MFGE8过表达似乎会加剧主动脉钙化。这突出了MFGE8介导的信号作为衰老血管钙化的新治疗靶点的潜力。据推测，年龄依赖性MFGE8表达的增加能够促进钙化和medin聚集。目的:1。探讨MFGE8是否促进血管钙化的发生。探讨MFGE8和钙化是否引起血管生理改变。确定与MFGE8介导的血管反应相关的信号通路。阐明medin是如何从MFGE8中分离出来的

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