Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to disseminate knowledge & skills of Acute Cardiovascular Care.
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
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 through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
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.
The ESC Councils' goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Prof. Johannes Waltenberger,
Novel insights into how smooth muscle cells (SMCs) are controlled greatly adds to our current understanding of atherosclerosis and plaque stability.The most recent and most exciting new concepts on vascular smooth muscle cell biology were presented and discussed in a dedicated symposium here at the 2013 ESC Congress in Amsterdam.Smooth muscle cells (SMCs) are major components of the arterial wall, as well as of the fibrous cap of the advanced atherosclerotic lesion. It has been known for years that uncontrolled proliferation of these cells leads to atherosclerotic plaque progression and the formation of stenotic lesions. Dr. C. De Vries from Amsterdam, NL, argued in her lecture on nuclear receptors in SMCs, that a reduced proliferation rate is likely to be deleterious as well, as the stability of the fibrous cap will be reduced and plaque rupture facilitated. Altogether, the regulation of SMC proliferation is a tightly regulated process involving a complex molecular machinery. Dr. P. Bouchet from Strasbourg, FR, extended on this notion focussing on the role of LRP, a representative from the LDL-receptor family, which activates the so called Wnt5a pathway and can trigger vascular calcification using Sox9 and Cart1.The behaviour of SMC is closely related to their differentiation state, as Dr. M-L Bochaton-Piallat from Geneva (CH) elucidated. She convincingly introduced S100A4 and Calmodulin as novel targets to modify SMC differentiation, with S100A4-inhibitors as well as the W7Cam-inhibitor being promising candidate molecules. Finally, Dr. M Bennett from Cambridge, UK, elaborated on the role of bone-marrow-derived SMC progenitor cells in arterial remodelling.Previous methodology using the detection of differentiation markers resulted in conflicting data. We now know that this is not the way to go anymore, while the use of genetic tracking of cells allow us to safely identify their origin and moreover, provides a basis for selective ablation, thereby modifying the atherogenic process.
Smooth muscle cells: friend or foe in atherosclerosis?
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