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Improving Health Through International Cardiovascular Research

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Improving Health Through International Cardiovascular Research 2014 NEWSLETTER Improving health through international 6 cardiovascular research Volume NEW TRANSATLANTIC NETWORKS P 2 Four new TNEs in 2014 and four TNEs in 2013 will increase the knowledge and improve the treatment of cardiovascular and neurovascular diseases. SCIENTIFIC ADVISORY COMMITTEE DEPARTURES AND ARRIVALS P 7 Three new members join the Scientific Advisory Committee in 2014 CALL FOR APPLICATION CYCLE 2014-2015 P 7 Due date is Friday, September 5, 2014, 11:59 pm Paris time LEDUCQ SYMPOSIUM 2015 P 7 The fifth Fondation Leducq Symposium will be held in Paris on April 16th, 2015. Sylviane Leducq (1925-2013) LEDUCQ FOUNDATION The Fondation Leducq mourns the passing of its founder and president, Sylviane Leducq, who TO BEGIN TO CONNECT along with her late husband Jean, inspired and NETWORKS supported so many in cardiovascular and neuro- P 7 Will set up vascular research. The FONDATION LEDUCQ NEWSLETTER is published once a year. Publication Director: David TANCREDI Editor: Sylvie LORAND-HULOT 1, rue Laurent Pichat • 75116 Paris • France Tel: +33 (0)1 45 00 59 65 • Fax: +33 (0)1 45 00 07 88 www.flcq.org ISSN 2103-7094 and brain, the proposed experiments and blood brain barrier permeability, genetically engineered mice. If successful will concentrate on genetic targeting network members propose specifically this group could help to launch a entirely 2014 of receptors and related pathways. to identify the cell types responsive new platform for the treatment of Building on a strong body of literature to SIP-mediated BBB regulation in neurovascular disease. implicating S1P in vascular regulation large part by the use of a variety of FONDATION LEDUCQ ANNOUNCES 2014 TRANSATLANTIC 3 Molecular Genetics, Pathogenesis and Protein-Replacement Therapy in NETWORKS OF EXCELLENCE AWARDS Arrhythmogenic Cardiomyopathy Four new Transatlantic Networks (TNE) received in September 2013, representing platform, which was introduced in the Ali Marian, The University of Texas, Houston, US and were selected by the Scientific a 30% increase in the number of cycle 2013-2014. William McKenna, University College of London , UK Advisory Committee (SAC) at its April LOIs received over the previous year. The networks awarded funding in 2014 2014 meeting in Napa Valley. These Submission now proceeds through a are : programs were chosen from among user-friendly online application service This network is designed to delineate normal structure and function and as the sharing expertise will have access to a 118 Letters of Intent (LOI) that were through the Altum proposalCENTRAL the molecular genetics, genomics, and disease progresses, there is ventricular well phenotyped AC patient popu- pathogenesis of arrhythmogenic cardio- dilation, dysfunction and aneurysm lation. They will continue searching 1 Deciphering the Genomic Topology of Atrial Fibrillation myopathy (AC). The classic right-dominant formation. Clinical heart failure is a late for new genes and new mutations, form of AC, known as arrhythmogenic manifestation. A switch in the fate and but most important of all, they will Patrick Ellinor, MGH, Boston, US and right ventricular cardiomyopathy, is a differentiation of a subset of cardiac investigate protein replacement in Vincent Christoffels, Academic Medical Center, Amsterdam, The Netherlands leading cause of sudden cardiac death resident cells to fibro-adipocyte is transgenic mouse models to attempt in young people. The burden of AC the pathological hallmark of AC. The to reverse the phenotype. The syner- is almost certainly underestimated, present challenge lies in elucidating gistic interactions between clinicians Atrial fibrillation (AF) affects over 3 have only a limited understanding the electrical rhythm of the heart? however, owing to frequent missed the intervening steps - from mutation and scientists in this network will million individuals in the US and 4.5 of mechanisms through which these Filling the gap of our understanding of diagnoses and under-recognition of the to pathologically overt disease - and ultimately improve the quality of life million individuals in Europe. Currently, genetic variants lead to AF. By combi- the molecular pathways underlying the left-dominant and biventricular subtypes. identifying therapeutic targets therein. and survival of AC patients. both medical and interventional ning deep insights into GWAS-signals, arrhythmia should ultimately provide Initially in this disease, the heart has a This network pooling resources and therapies for AF are only partially knowledge of the 3D topology of the new diagnostic tools and therapeutic effective, and are associated with human genome, and expertise in the strategies to reduce the unacceptable substantial morbidity. Although recent translation of genetic changes, the burden of stroke, death, and hospita- genome-wide association studies members of this network will address lizations associated with this common (GWAS) have identified over a dozen the major question in AF genetics: arrhythmia. 4 Programming the failing heart to a regenerative state genetic loci associated with AF, we how do the genetic mutations affect Richard Lee, Brigham & Women Hospital, Cambridge, US and Mauro Giacca, ICGEB, Trieste, Italy 2 SphingoNet - Sphingosine 1-Phosphate in Neurovascular Biology and Disease Given the global burden of heart fate in vitro and in vivo, improving of repair mechanisms, they will define disease and its increasing prevalence cardiac function and reducing adverse and optimize methods for enhancing Timothy Hla, Cornell University, New York, US and in aging populations, one of the most ventricular remodeling, this network function of injured mammalian hearts, Christer Betsholtz, Uppsala University, Sweden important challenges of modern will use a combination of factors, and will extend these studies to a large medecine is the development of including microRNAs, to reprogram animal model to bring this know- strategies to regenerate the human adult human fibroblasts into cardio- ledge toward translation, in mini-pigs, Understanding the control and system function to focus on the central and has been found to be effective in heart. This network is focused on myocyte-like cells. The members of non-human primates and human regulation of the BBB is of significant role of sphingosine 1-phosphate (S1P) multiple sclerosis. The network project promoting the regenerative poten- this network will collaboratively develop engineered myocardium. This line of clinical importance because the BBB in the development and regulation will further characterize the role of tial of endogenous cells of the heart a series of interrelated strategies to research should provide new therapeutic remains one of the major obstacles of the neurovascular unit and blood S1P in ischemia. When dysregulated, a different strategy from that found enhance cardiac regeneration and approaches to enhance the limited in the delivery of drugs to the central brain barrier (BBB) in health and S1P signaling causes neuroinflammation in many stem cell programs where repair by the reprogramming of capacity of the heart to regenerate, nervous system. The transatlantic disease. This is a novel approach to the and neurovascular disease. As very exogenous cells are added to produce non-cardiac cells, like macrophages, having applications in diverse cardiac network led by Christer Betsholtz and investigation of the neurovascular unit little is known about S1P and its receptor a therapeutic effect. Building on the into cardiomyocytes and by promoting disorders, including both genetic and Timothy Hla brings together experts in prompted by the discovery of a drug systems that are expressed on multiple finding that mouse fibroblasts can be the homing of cardiac regenerating acquired forms of heart disease. blood vessels, immunology and nervous that influences sphingosine signaling cell types and tissues in vessels reprogrammed toward a cardiac cell cells. Through activation and stimulation 2 3 disease, which may provide additional vascular diseases. With the finding that clinically relevant, large animal models prognostic information over what can newly-discovered non-coding RNAs as a pathway to first-in-man clinical 2014 be gained from established risk factors are associated with vascularization, trials to treat human disease. and co-morbidities. atherosclerosis and aneurysm formation, The diverse and synergistic talents of Surprisingly, the cellular source and researchers now believe that vascular the investigative team will provide an functional significance of circulating miRNAs are central targets for thera- unprecedented, comprehensive approach miRNAs in vascular disease are still peutic manipulation. The network will towards understanding the biological unknown. Determining the importance focus on new and previously identified role and therapeutic potential of FONDATION LEDUCQ 2013 TRANSATLANTIC NETWORKS of miRNAs as novel cell/cell communi- candidate miRNAs as potential therapies miRNAs. This networking and training cators may allow for the development for these three vascular disease areas strategy on vascular miRNAs will signi- OF EXCELLENCE AWARDS of biomarker profiles based on circulating using genetically modified animal models ficantly contribute to future diagnostic mi-RNAs. The central aim of this and pharmacologic strategies. and therapeutic benefits for patients Four Transatlantic Networks (TNE) were selected by the Scientific Advisory Committee (SAC) at its April 2013 meeting in Nice. project, however, is to
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