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      Meeting report from the 2nd International Symposium on New Frontiers in Cardiovascular Research. Protecting the cardiovascular system from ischemia: between bench and bedside

      research-article
      , , , , , , , , , , , , , , , , , , , , , , , , , ,
      Basic Research in Cardiology
      Springer Berlin Heidelberg
      Atherosclerosis, Cardioprotection, Cardiovascular disease, Endothelial permeability, Extracellular RNA, High-density lipoprotein, Hypoxia, Inflammation, Ischemia/reperfusion injury, Macrophage polarization, MicroRNAs, Mitochondria, Platelet dysfunction, Vascular biology

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          Abstract

          Recent advances in basic cardiovascular research as well as their translation into the clinical situation were the focus at the last “New Frontiers in Cardiovascular Research meeting”. Major topics included the characterization of new targets and procedures in cardioprotection, deciphering new players and inflammatory mechanisms in ischemic heart disease as well as uncovering microRNAs and other biomarkers as versatile and possibly causal factors in cardiovascular pathogenesis. Although a number of pathological situations such as ischemia–reperfusion injury or atherosclerosis can be simulated and manipulated in diverse animal models, also to challenge new drugs for intervention, patient studies are the ultimate litmus test to obtain unequivocal information about the validity of biomedical concepts and their application in the clinics. Thus, the open and bidirectional exchange between bench and bedside is crucial to advance the field of ischemic heart disease with a particular emphasis of understanding long-lasting approaches in cardioprotection.

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          Most cited references112

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          Mitofusin 2 tethers endoplasmic reticulum to mitochondria.

          Juxtaposition between endoplasmic reticulum (ER) and mitochondria is a common structural feature, providing the physical basis for intercommunication during Ca(2+) signalling; yet, the molecular mechanisms controlling this interaction are unknown. Here we show that mitofusin 2, a mitochondrial dynamin-related protein mutated in the inherited motor neuropathy Charcot-Marie-Tooth type IIa, is enriched at the ER-mitochondria interface. Ablation or silencing of mitofusin 2 in mouse embryonic fibroblasts and HeLa cells disrupts ER morphology and loosens ER-mitochondria interactions, thereby reducing the efficiency of mitochondrial Ca(2+) uptake in response to stimuli that generate inositol-1,4,5-trisphosphate. An in vitro assay as well as genetic and biochemical evidences support a model in which mitofusin 2 on the ER bridges the two organelles by engaging in homotypic and heterotypic complexes with mitofusin 1 or 2 on the surface of mitochondria. Thus, mitofusin 2 tethers ER to mitochondria, a juxtaposition required for efficient mitochondrial Ca(2+) uptake.
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            Third universal definition of myocardial infarction.

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              Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

              Circulation, 74(5), 1124-1136
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                Author and article information

                Contributors
                +65 66015121/65166719 , derek.hausenloy@duke-nus.edu.sg
                Journal
                Basic Res Cardiol
                Basic Res. Cardiol
                Basic Research in Cardiology
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0300-8428
                1435-1803
                14 December 2015
                14 December 2015
                2016
                : 111
                : 7
                Affiliations
                [ ]Institute of Biochemistry, Medical School, Justus-Liebig University, Giessen, Germany
                [ ]Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore, Singapore, Singapore
                [ ]National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore
                [ ]Department of Microbiology, Kazan Federal University, Kazan, Russian Federation
                [ ]Escuela de Ingeniería y Ciencias, Centro de Biotecnología-FEMSA, Tecnológico de Monterrey, Monterrey, NL México
                [ ]Institute of Genetics, Univeristy of the Sea. Puerto Escondido Campus, Oaxaca Oaxacan System of State Universities (SUNEO), Oaxaca, México
                [ ]Research Unit, Hospital of Santa Cristina, Research Institute Princesa (IP), Autonomous University of Madrid, Madrid, Spain
                [ ]Institute of Biochemistry and Molecular Cell Biology, RWTH Aachen University, Aachen, Germany
                [ ]Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, USA
                [ ]Department of Cardiology, Aarhus University Hospital, Skejby, Aarhus N, Denmark
                [ ]Department of Hematology, Instituto Nacional de Cancerología, Mexico City, Mexico
                [ ]Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe-University, Frankfurt, Germany
                [ ]Valld’Hebron University Hospital and Research Institute, Barcelona, Spain
                [ ]Hatter Institute and MRC Inter-University Cape Heart Unit, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa
                [ ]Institute for Molecular Cardiovascular Research, RWTH University Hospital Aachen, Aachen, Germany
                [ ]Department of Cardiology, The Rayne Institute, St Thomas’ Campus, King’s College London, London, UK
                [ ]Department of Clinical Pharmacology, University College London, London, UK
                [ ]The James Black Centre, King’s College, University of London, London, UK
                [ ]Department of Molecular Biology, National Institute of Cardiology, Mexico City, Mexico
                [ ]Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
                [ ]Laboratorio de Biofísica Cardiaca, Instituto de Fisiología, Universidad Autónoma de Puebla, Puebla, Mexico
                [ ]Institute of Anatomy and Vascular Biology, Westfalian-Wilhelms-University, Münster, Germany
                [ ]Laboratory of Parasitology, Department of Microbiology and Parasitology, Faculty of Medicine, Universidad Nacional Autónoma de México, Mexico City, Mexico
                [ ]Laboratorio Multidisciplinario de Ciencias Biomédicas, Instituto de Investigaciones Medico-Biológicas, Universidad Veracruzana campus Veracruz, Veracruz, Mexico
                [ ]Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu, USA
                [ ]The Hatter Cardiovascular Institute, University College London, London, UK
                [ ]The National Institute of Health Research University College London Hospitals Biomedical Research Centre, London, UK
                Article
                527
                10.1007/s00395-015-0527-0
                4679108
                26667317
                e09376d7-c2dc-4e03-9d61-e61259380c88
                © The Author(s) 2015

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 26 November 2015
                : 26 November 2015
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                © Springer-Verlag Berlin Heidelberg 2016

                Cardiovascular Medicine
                atherosclerosis,cardioprotection,cardiovascular disease,endothelial permeability,extracellular rna,high-density lipoprotein,hypoxia,inflammation,ischemia/reperfusion injury,macrophage polarization,micrornas,mitochondria,platelet dysfunction,vascular biology

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