Mechanisms of early vascular lesions : endothelial dysfunction and arterial calcification
This WP will build up on the recognized expertise of the Amiens and Rouen groups in the fields of detection, mechanistic analysis and treatment of calcification (Amiens) and of endothelial dysfunction (Rouen).
Vascular calcification (VC) is a common disease in aging, frequently encountered in general population although its prevalence is much higher in diabetes and overall in patients with chronic kidney disease (CKD) where it is associated with an elevated cardiovascular mortality. Two major types of VC are distinguished: intimal calcifications which develop within atheromatous plaque and frequently aggravate the atherosclerotic process, and medial calcification (Monckeberg’s sclerosis) causing arteriosclerosis that can lead to vascular stiffness and which is frequently observed in CKD patients. The mechanisms involved in VC are very complex and depend on a balance between pro-calcifying factors and inhibitors of calcification. Our main scientific objectives will be to address:
1 - The molecular and cellular mechanisms involved in VC and endothelial dysfunction
2 - The hemodynamic and structural consequences of VC and endothelial dysfunction
3 - The factors or markers associated with VC and endothelial dysfunction
4 - New therapeutic strategies to prevent and treat VC and endothelial dysfunction