Grant: CIHR Fellowship

Aortic stenosis (AS) is a pathology afflicting aortic valves and having many similarities with atherosclerosis. Histological features of AS suggest a chronic inflammation that culminate with a proeminent calcification of aortic valves. At this time, aortic valve replacement is the only available solution for patients suffering from AS. However, our group has recently obtained results suggesting the possibility to develop medication for patients suffering from AS.Indeed, we have demonstrated that administration of ApoA-I mimetic peptide can induce the regression of valvular calcification. However, the mechanism by which this peptide induces this effect remains unknown. Given that ApoA-I is a main component of HDL, these results suggest that lipoproteins could be implicated in the regression of calcification. However, to our knowledge, there are actually no studies on this topic. Thus, our hypothesis is that HDL have the ability to prevent and regress valvular calcification by influencing anti-calcifying proteins and osteoclast-like cells. We are confident that the understanding of events leading to activation or inhibition of osteoclast activity in this illness will be helpful for the elaboration of therapeutic strategies. Moreover, since AS has many similarities with atherosclerosis, the understanding of AS could also serve benefit the treatment of atherosclerosis. Given the social importance of this research and the high therapeutic potential, we are confident that results will lead to high quality publications.