< Back to previous page

Project

In depth investigation of causal pathophysiological mechanisms and underlying molecular signaling pathways of arterial stiffness, a life threatening disease with serious impact on multiple organs.

Arterial stiffening is a hallmark of vascular aging and is associated with a high risk of cardiovascular disease and end-organ failure in kidney and brain (dementia). No effective therapies to combat this life threatening pathology currently exist, which is largely due to the lack of knowledge of the underlying molecular mechanisms. Therefore, this project aims to identify novel druggable targets which opens up new perspectives for discovery and evaluation of inventive therapies for this growing epidemic. Endothelial dysfunction and vascular calcification are two well known pathological processes leading to arterial stiffness. Established mouse models of both will be used to identify the molecular signaling pathways responsible for arterial stiffness by use of quantitative proteomics coupled with bioinformatic analysis. We will also explore the reciprocal relationship between different pathological processes leading to arterial stiffness. As impaired autophagy has been suggested to play a role in vascular aging, this project will also focus on its role in vascular calcification and stiffness. To explore whether autophagy is a candidate target for future intervention studies, complementary in vivo studies will be performed that investigate the effect of both autophagy induction and deficiency on vascular calcification and stiffness. Ultimately, this project aims to prevent or possibly reverse stiffening of large arteries to reduce long-term risk for end-organ damage.
Date:1 Jan 2020 →  31 Dec 2023
Keywords:VASCULAR SMOOTH MUSCLE CELLS, VASCULAR CALCIFICATION, VASCULAR DISEASE, VASCULAR ENDOTHELIUM
Disciplines:Biomarker discovery, Drug discovery and development not elsewhere classified, Vascular diseases, Cardiac and vascular medicine not elsewhere classified