SFB 1123 Atherosclerosis-Mechanisms and Networks of Novel Therapeutic Targets
print


Breadcrumb Navigation


Content

Projects Area C: associated projects

C01: Mechanisms of inflammation-driven atheroprogression after stroke

Secondary cardiovascular events after acute stroke are contribute substantially to post-stroke morbidity. We recently demonstrated that stroke promotes progression of atherosclerosis and consequently hypothesize that plaque myeloid cell expansion secondary to stroke is a druggable mechanism promoting atheroprogression and resulting in recurrent cardiovascular events. We aim to characterize changes in plaque leukocyte composition after stroke (Aim 1), determine the origin of plaque leukocytes after stroke (Aim 2), test post-stroke exacerbation of atherosclerosis (Aim 3), and analyze leukocyte numbers/phenotypes in human endarterectomy and blood samples (Aim 4).

C02: Exploring crosstalk between lipids, complement and neurovascular interfaces in unresolvable inflammation 

Secondary cardiovascular events after acute stroke are contribute substantially to post-stroke morbidity. We recently demonstrated that stroke promotes progression of atherosclerosis and consequently hypothesize that plaque myeloid cell expansion secondary to stroke is a druggable mechanism promoting atheroprogression and resulting in recurrent cardiovascular events. We aim to characterize changes in plaque leukocyte composition after stroke (Aim 1), determine the origin of plaque leukocytes after stroke (Aim 2), test post-stroke exacerbation of atherosclerosis (Aim 3), and analyze leukocyte numbers/phenotypes in human endarterectomy and blood samples (Aim 4).

C03: Assessing novel therapeutic strategies in genetically mutated mini-pig models of atherosclerosis


Translation of pre-clinical therapeutic strategies into patient-relevant therapies remains an obstacle. To improve this, we aim to advance preclinical models of cardiovascular disease and thereby to enhance bench-to-bedside translation. Specifically, we will characterize different mini-pig models of atherosclerosis (Aim 1). Subsequently, we will investigate the efficacy of DNA/RNA based therapies in the atherosclerotic vasculature (Aim 2). A therapeutic approach for cardiac improvement will be performed via miR-92a modulation (Aim 3), while carotid plaque vulnerability will be tested upon modulation of miR-210 and the long non-coding RNA MIAT (Aim 4).