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During ESC Congress, the Working Group on Atherosclerosis and Vascular Biology awards two young investigators (under 36) who submitted the best abstract on Atherosclerosis and the best abstract on Vascular Biology.
Abstracts ranking is based on the marks awarded by the ESC abstract reviewers and by the Working Group leadership.
Nanoparticle-mediated simultaneous targeting of mitochondria and inflammatory monocytes protects the brain from ischemia-reperfusion injury in mice
Who are you?
My name is Arihide Okahara. I am 33 years old. I graduated as a medical doctor from Kyushu University in 2010 and I had worked as a cardiologist for 5 years. In 2015 I started my research life at the Department of Cardiology, Kyushu University, Fukuoka, Japan.
What got you interested in research?
Through the clinical experience as a cardiologist, I have realized that some patients would not recover by current medical treatments and there are unmet medical needs. I would like to satisfy the unmet needs and save the life of future patients by my research, therefore I have selected the way of research.
What question your study addressed and how do you interpret your findings?
Ischemic stroke is a major cause of death and loss of QOL. Recently, reperfusion therapy has become a common procedure, but its therapeutic effect is hampered by ischemia-reperfusion (IR) injury. Opening of mitochondrial permeability transition pore (mPTP) is one of the major mechanisms of IR injury, but pharmacological inhibition of mPTP opening failed to ameliorate patients’ outcome. We have developed nanotechnology-based drug delivery system using bioabsorbable polymer, poly (lactic-co-glycolic acid) (PLGA) and found that nanoparticle-mediated delivery of cyclosporine A, an inhibitor of mPTP opening, decreases infarct size after IR injury. However, we found that inhibition of mPTP opening did not have the significant effect on inflammation and CypD/CCR2 double knockout showed the striking reduction of infarct size as compared to single knockout. Similarly, an additional targeting of inflammation by nanoparticle-mediated delivery of HMG-CoA inhibitor further decreased infarct size. These results suggest that our drug delivery system could be a novel and innovative strategy for the treatment of cerebral IR injury.
What does winning the “Young Investigator Award” for best abstract on Atherosclerosis / Vascular Biology at the ESC 2018 mean to you, and to your future?
This is the first time for me to win such an international honorable prize, so I was very pleased to be selected the “Young Investigator Award” for best abstract on Atherosclerosis / Vascular Biology at the ESC 2018. I would like to thank the ESC Working group. I am fortunate to be blessed with my mentor Prof. Kensuke Egashira, Dr. Tetsuya Matoba, Dr. Jun-ichiro Koga and my colleagues at Kyushu University and would like to express my appreciation to them. This award encouraged and motivated me for future research. I would like to continue enjoying my research!
Stat4 deficiency exacerbates atherosclerosis through promoting foam cell formation via pi3k/akt/nfkb/mir-9/acat1 pathway in ApoE-/- mice
My name is Lili Xu. In 2016 I graduated as a medical doctor from Shanghai Medical College, Fudan University. Now I’m working as an attending physician in Cardiology Department of Zhongshan Hospital, Fudan University in Shanghai.
I chose cardiology as my career because of its vital importance to people’s lives as well as its complex pathophysiology that challenges and excites me. Doing research can improve our knowledge of the underlying mechanism of diseases.
We show that genetic deletion of STAT4 promotes the differentiation of pro-inflammatory M1 macrophages from CD11b+Gr-1+ myeloid cells and leads to enhanced atherosclerotic lesion formation in ApoE-/- mice. Deficiency of STAT4 caused the inhibition of PI3K/Akt signal, the less nuclear translocation of NFκB, subsequent down-regulated transcription of miR-9 and ultimate up-regulation of ACAT-1, which has been reported to promote the formation of macrophages-derived lipid-laden foam cells. We have characterized a novel role for STAT4 signal in modulating innate immune response and atherogenesis. Moreover, our work has figured out the detailed mechanisms by which STAT4 regulates the progress of atherosclerosis.
I feel very honored to receive the young investigator award. Winning this award in my early career could give me some motivation to continue my research and keep doing best in the future. Again I would like to thank the working group for acknowledging our work.
Endoplasmic reticulum protein thioredoxin domain containing 5 (TXNDC5) is a novel mediator of endothelial dysfunction and atherosclerosis
My name is Shih-Hsin Cheng. In 2016, I graduated as a pharmacist from China Medical University in Taiwan. I am currently a graduate student at Prof. Kai-Chien Yang’s lab in the Graduate Institute and Department of Pharmacology, National Taiwan University (NTU) School of Medicine.
Starting from the undergraduate period, I was deeply fascinated by cardiovascular physiology. After enrolling in the graduate program at NTU, I decided to join Prof. Yang’s lab to study the role of TXNDC5 in the pathogenesis of endothelial dysfunction and atherosclerosis, which is a collaborative project with Dr. Chih-Fan Yeh in NTU hospital and Prof. Yun Fang in U of Chicago. Although there has been ups and downs while working on this project, research has brought me the joy of exploring the undiscovered edge of cardiovascular medicine.
Atherosclerotic cardiovascular diseases (ASCVD) are the leading causes of death worldwide and current pharmacotherapy is limited to prevent the progression of the disease. It is, therefore, critical to identify novel mediators of atherosclerosis to develop new therapeutic approach to treat or prevent ASCVD. In our study, TXNDC5 was found to be highly upregulated in endothelial cells under atherogenic stimuli, including disturbed flow and hyperlipidemia. In addition, TXNDC5 was also significantly increased in the atherosclerotic plaques/endothelium in human as well as in ApoE-/- mice fed with high fat diet (HFD). Importantly, targeted deletion of Txndc5 in ApoE-/- mice markedly reduced the aortic plaque areas following HFD and carotid atherosclerosis following partial carotid artery ligation. Mechanistically, the downregulation of endothelial eNOS observed in ApoE-/- mice was normalized with the deletion of Txndc5, suggesting that Txndc5 deletion/inhibition could be protective against atherosclerosis by raising endothelial eNOS levels. Targeting TXNDC5, therefore, could be a novel therapeutic approach to treat or prevent ASCVD.
What does winning the “Young Investigator Award” for best abstract on Vascular Biology at the ESC 2018 mean to you, and to your future?
It was my great honor to win the prestigious Young Investigator Award selected by the ESC Working Group on Atherosclerosis and Vascular Biology. It means a lot to me as a junior graduate student working in this important yet competitive field. I am grateful for the guidance and support from my mentor and colleagues. Winning this award definitely encourages me to work harder and motivates me to keep on pushing this project forward and contribute to this field.
Left to the right: Magnus Back, Cristian Weber, Daniel Ketelhuth, Imo Hoefer, Sharda Suzan Anroedh, Jochen Dutzmann, Paul Evans, Marie-Luce Bochaton-Piallat, Jose Tunon.
Serum PCSK9 in relation to coronary near-infrared spectroscopy-derived lipid core burden index and long-term cardiovascular outcome [ATHEROREMO-NIRS substudy]
My name is Sharda Suzan Anroedh. In 2012 I graduated as a medical doctor from the University Medical Center Rotterdam (Erasmus MC). At the end of 2014, I started my PhD at the Department of Cardiology/Epidemiology, Erasmus Mediaal Center.
I chose for research, because only research can improve our knowledge. We need research to go beyond where we are now. Furthermore I chose cardiology because I’m very interested in the heart/vascular system more than other systems, partially because of its vital importance to people's lives. Cardiology can be life and death. It feels good to know that in some way, I am helping and that one day in the future my research might even save or improve lives.
Can we identify and prevent a vulnerable plaque from rupture in patients with coronary artery disease? With this question in mind we started the AtheroRemo study. In this study we investigated the association between serum PCSK9 levels and Lipid Core Plaque (LCP), as assessed by NIRS, in a non-culprit coronary artery in 203 patients and the association between serum PCSK9 levels and the occurrence of clinical cardiovascular outcome during long-term follow-up over 4.7 years in 581 patients undergoing CAG because of ACS or SAP. Serum PCSK9 level is associated with amount of lipid core in coronary atherosclerosis as assessed by NIRS. NIRS has the potential to identify LCPs that is indicative of plaque vulnerability in the coronary arteries. So, in this context PCSK9 may be used to select patients with a vulnerable plaque to measure the effect of medical decision and the management of lipids in secondary prevention.
What does winning the “Young Investigator Award” for best abstract on Atherosclerosis at ESC Congress 2017 mean to you and to your future?
The Award ‘for best abstract on Atherosclerosis at ESC Congress 2017’ is my first international prize for research and a major step in my career. My knowledge of the topic I am working on so far have surely been improved and strengthened by the achievement of the ESC Young Investigator Award. I have benefited substantially from the contest in terms of personal development but also mainly on my carrier possibilities. The award also gave me some extra motivation to do my best in my research career. It was a great moment when the award was announced in front of highly respected audience during the award ceremony. My colleagues and supervisors are very proud of this achievement. This achievement would not be possible without the excellent supervision of my seniors and support from the Department of Cardiology, University Medical Center Rotterdam.
Adventitial cytokine production is critical for negative vascular remodelling
I am a 31-year-old clinician scientist at the Dept. for Cardiology and Angiology of the Hannover Medical School combining clinical work at our acute cardiac care unit and scientific work at the Vascular Remodeling and Regeneration group of Professor Daniel Sedding. Beside my medical studies in Giessen, Germany, I deepened my clinical education at the University Hospital of Basel, Switzerland and got the opportunity to broaden my scientific mind through a research fellowship at the lab of Professor Peter Libby at the Harvard Medical School/Brigham and Women’s Hospital in Boston, MA, USA. I am married to a pediatrician and father of two daughters (1 and 3 years old).
In Germany, carrying out a research project is required to earn a MD degree. Therefore, I applied for a MD student position at the lab of Professor Daniel Sedding at the Hannover Medical School and got the opportunity to participate in a project entitled “Impact of STAT3 on smooth muscle cell proliferation and neointima formation“. I became part of a close-knit and delightful group, had an enlightening time, and took part in other research projects of the group. After graduating from the University of Gießen Medical School, Professor Sedding accepted a position as a Professor for Vascular Remodeling and Regeneration at the Hannover Medical School and asked me to support the set up of his working group in Hannover.
What question does your study address and how do you interpret your findings?
In our lab, we use a mouse model of femoral artery dilation to investigate the pathogenesis of negative vascular remodeling processes. Throughout our research projects, we incidentally found high adventitial proliferation rates early following wire-induced injury. To proof, whether this was either just a side effect or a high-impact finding, we surgically removed the adventitial layer following wire-induced injury. Remarkably, mice without a femoral artery adventitial layer exhibited a significantly reduced neointimal lesion size. The high impact of the adventitial layer to neointimal lesion formation was due to an indirect paracrine contribution rather than a direct cellular contribution as investigated by transplantation of an ubiquitously GFP-expressing adventitia around the femoral medial layer of WT mice. Incubation of activated adventitial grafts in serum-free media and subsequent secretome analysis revealed remarkably high interleukin-6 levels. Conclusively, transplantation of an interleukin-6 negative adventitia around the femoral medial layer of WT mice prevented neointimal lesion formation.
With this study, we provide evidence for the high and extensive impact of the adventitial layer in negative vascular remodeling processes for the first time. Thereby, we did the groundwork for future studies, which may follow to investigate treatment options involving cellular adventitial processes.
What does winning the “Young Investigator Award“ for the best abstract on Vascular Biology at ESC Congress 2017 mean to you and to your future?
Winning the “Young Investigator Award“ is a great appreciation of my scientific work by experienced and renowned scientists of the field. It definitely encourages me as a young investigator to further pursue ideas, especially those that might be somewhat risky even though innovative.
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
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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