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Our mission is to promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our mission is to reduce the burden of cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our mission is to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
During the Working Group General Assembly at ESC Congress 2016, the ESC Working Group on Atherosclerosis and Vascular Biology has given awards to two young researchers: one for the best abstracts on Atherosclerosis and the other one for the best abstract on Vascular Biology.
Best abstracts ranking is based on the marks awarded by the ESC abstract reviewers and by the Working Group leadership.
Jolanda Wentzel, Magnus Back, José Tunon, Claudia Monaco, Daniel Ketelhuth, Kira Kuschnerus, Tasneem Arsiwala, Paul Evans, Imo Hoefer, Christian Weber [left to the right]
Bone marrow-specific Sirt6 deletion enhances atherosclerosis and foam cell formation via an increase in macrophage scavenger receptor 1 expression
Interview:My name is Tasneem Arsiwala. I am a doctoral student at the Center for Molecular Cardiology, University of Zurich, investigating the role of aging genes like Sirtuin 6 on atherosclerosis. I completed my Bachelor’s degree in Pharmacy from the University of Mumbai and I went on to get a Master of Science in Pharmacology from the University of Oxford.
I have always been fascinated by the action of medicines on the human body and how they can treat diseases. This led me to study pharmacy and then pharmacology. Ever since I have been enthralled by how complex pathophysiology really is and I enjoy the challenge and excitement to investigate the pathways underlying disease progression.
The goal of my project was to elucidate the mechanistic underpinnings of Sirt6 regulation and its role in atherogenesis. In my project we show how the bone-marrow specific deletion of Sirt6 proatherosclerotic. There is an increase in macrophage scavenger receptor 1 (Msr1) and we can conclude that macrophage-derived Sirt6 is atheroprotective via the regulation of Msr1.
I am very pleased to receive the “Young Investigator Award” for best abstract on Atherosclerosis / Vascular Biology. I would like to thank the ESC Working group for giving me this award and recognizing my work. I would like to continue doing similar exciting projects on research that has the potential to be translational. This award is very encouraging to a young researcher like me and it motivates me to continue to giving my best and enjoying my work.
The microRNA miR-483-3p affects vascular response to injury by promoting endothelial cell apoptosis
Interview:I am a physician scientist in the Department of Cardiology at Charité Berlin (chief: Prof. Ulf Landmesser).
Doing research was actually a kind of experiment for me. During medical school in Hannover, Germany, I decided to pursue an experimental doctoral thesis with Ulf Landmesser at the University of Zurich. At that point I did not know if basic research was something I wanted to engage in later on in my career. However, it occurred to me, that if you want to get a proper impression of what doing basic research means, you cannot do in parallel to studying medicine. So I took a leave of absence from med school and stayed in the Zurich lab for one and a half years of laboratory work.
My study addresses the role of micro-RNA-483-3p in the response to vascular injury with a special focus on patient with coronary artery disease (CAD) and type 2 diabetes (T2D). miR-483-3p induces cell death in a circulating endothelial regenerative cell population (EOCs, early outgrowth cells) in patients with CAD and concomitant T2D as well as in human aortic endothelial cells (HAEC). As cardiovascular risk morbidity and mortality is excessively high in this patient population we wondered whether miR-483 might be mechanistically involved in diabetic vascular disease. We could demonstrate that miR-483 overexpression lead to a reduced endothelial repair capacity in vivo. Likewise, inhibition of miR-483-3p expression by an anti-miR in EOCs of CAD+T2D patients rescued their ability to support endothelial repair in vivo. In an animal model of type 2 diabetes and obesity, systemic application of anti-miR against miR-483-3p effectively reduced miR-483-3p expression in the vasculature which was associated with improved endothelial repair after artificial vascular injury. We therefore hypothesize, that miR-483-3p is involved in the unfavourable vascular phenotype of type 2 diabetic CAD patients and that targeting this microRNA might hold therapeutic potential in the treatment of patients with CAD and T2D in the future.
I would like to thank the working group for acknowledging my work with a Young Investigator Award. Especially with my background as a clinician, I feel honoured, that the committee appreciated my work to be of high scientific quality. Personally, I feel that if as a clinician you pursue a parallel career in basic science, it always comes at a cost. In the clinic, you are not proceeding as quickly as your peers if you devote a lot of your time to basic research. However, in science, you also have to invest a lot of time to stay up to date on current scientific knowledge and methodology in order to remain competitive. Therefore, receiving the Young Investigator Award encourages me to carry on in my endeavour to make clinical and scientific ends meet when I move on to clinical specialty training in cardiac surgery in the German Heart Center in Berlin.
Claudia Monaco, Kosta Theodorou, Imo Hoefer / Claudia Monaco, Norifumi Nishida, Imo Hoefer [left to the right]
Loss of endothelial ADAM10 augments atherosclerosis development in mice
Excessive sodium intake worsens aortic dissection via IL-17 pathway
The Working Group wishes to express its sincere appreciation to sponsors who have supported the initiative and the outstanding scientific work of the awardees:
Erik Walter Holy, Christian Weber (Working Group Chaiman) and Iwai Ryosuke [left to the right]
Astract: “Carbamylated LDL induces a pro-thrombotic state via the LOX-1 receptor and arterial thrombus formation: a novel mechanism of cardiovascular events in end-stage renal disease”
Retrieve the interveiew of Erik Walter Holy
Abstract : “Rapid in vivo maturation of BIOTUBE vascular grafts by giant drops patching of adipose-derived stromal cells (ADSCs)”
Retrieve the interview of Iwai Ryosuke
The Working Group on Atherosclerosis and Vascular Biology wishes to express its sincere appreciation to sponsors who have supported the initiative and the outstanding scientific work of the awardees.
Rob Krams, Susanna Sluka, Konstantin Stark, Claudia Monaco and Christian Weber [left to the right]
Abstract: "Tissue factor disulfide mutation causes a bleeding phenotype with gender specific organ pathology and lethality"
Abstract: "Neutrophils contribute to DVT formation by forming procoagulant and prothrombotic neutrophil extracellular traps"
The Working Group on Atherosclerosis and Vascular Biology wishes to express its sincere appreciation to sponsors who have supported the initiative and the outstanding scientific work of the awardees:
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