Arterial stiffness has long been recognized as a feature of arterial aging. Recently, arterial stiffness has received increasing attention in cardiovascular medicine, emerging as an independent risk factor for cardiovascular disease and mortality. Additionally, patients with highly prevalent metabolic disorders, such as diabetes mellitus, feature a dramatically increased cardiovascular risk coming along with accelerated arterial stiffening. As such, the group’s major interests are to delineate the molecular mechanisms leading to increased arterial stiffness and to better understand the pathomechanistic role of arterial stiffness in specific cardiovascular

diseases (such as atherosclerosis, aortic aneurysm/dissection, heart failure and stroke). As a result, we seek to define novel pharmaceutical targets to prevent arterial stiffening processes as well as develop strategies to reduce biomechanical stress arising from adverse vascular remodeling. As part of our functional studies we are employing in vivo vascular ultrasound methods, ex vivo material testing (pressure myography) as well as computer-based finite elements analysis (FEA).

Non-coding RNAs (such as microRNAs, long non-coding RNAs) have recently attracted much attention not only as a novel class of gene and disease regulators but also as attractive targets for pharmaceutical intervention. In various projects the group is addressing the role of ncRNAs as mechanosensitive regulators of distinct vascular pathologies (such as aortic aneurysms, atherosclerosis, or age-related arterial stiffness).

Employing a comprehensive approach using human biobank materials as well as in vitro, in vivo and bioinformatical models we identify ncRNAs potentially involved in disease pathophysiology, taking advantage of latest profiling technologies (such as RNAseq). Subsequently, selected ncRNAs are subjected to rigorous mechanistic studies in vitro as well as in vivo to validate their utility as therapeutic targets.