28
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      From basic mechanisms to clinical applications in heart protection, new players in cardiovascular diseases and cardiac theranostics: meeting report from the third international symposium on “New frontiers in cardiovascular research”

      review-article
      1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 4 , 10 , 11 , 2 , 3 , 33 , 2 , 3 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 2 , 3 , 35 , 33 , 34 , 21 , 22 , 23 , 24 , 25 , 26 , 2 , 3 , 27 , 28 , 2 , 3 , 29 , 30 , 31 , 3 , 6 , 32 , 33 , 6 , 33 , 34 , 2 , 3 , 33 , 34 , , 1 , 4
      Basic Research in Cardiology
      Springer Berlin Heidelberg
      Cardiomyocyte signaling pathways, Cardioprotection, Cardiovascular disease, Co-morbidities, Drug targeting, Endothelial permeability, Extracellular RNA (eRNA), Heart regeneration, Induced pluripotent stem cells, Ischemia–reperfusion injury, Lipid metabolism, MicroRNAs (miRNAs), Mitochondria, Remote ischemic conditioning

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          In this meeting report, particularly addressing the topic of protection of the cardiovascular system from ischemia/reperfusion injury, highlights are presented that relate to conditioning strategies of the heart with respect to molecular mechanisms and outcome in patients’ cohorts, the influence of co-morbidities and medications, as well as the contribution of innate immune reactions in cardioprotection. Moreover, developmental or systems biology approaches bear great potential in systematically uncovering unexpected components involved in ischemia–reperfusion injury or heart regeneration. Based on the characterization of particular platelet integrins, mitochondrial redox-linked proteins, or lipid-diol compounds in cardiovascular diseases, their targeting by newly developed theranostics and technologies opens new avenues for diagnosis and therapy of myocardial infarction to improve the patients’ outcome.

          Related collections

          Most cited references113

          • Record: found
          • Abstract: found
          • Article: not found

          Thrombosis as an intravascular effector of innate immunity.

          Thrombosis is the most frequent cause of mortality worldwide and is closely linked to haemostasis, which is the biological mechanism that stops bleeding after the injury of blood vessels. Indeed, both processes share the core pathways of blood coagulation and platelet activation. Here, we summarize recent work suggesting that thrombosis under certain circumstances has a major physiological role in immune defence, and we introduce the term immunothrombosis to describe this process. Immunothrombosis designates an innate immune response induced by the formation of thrombi inside blood vessels, in particular in microvessels. Immunothrombosis is supported by immune cells and by specific thrombosis-related molecules and generates an intravascular scaffold that facilitates the recognition, containment and destruction of pathogens, thereby protecting host integrity without inducing major collateral damage to the host. However, if uncontrolled, immunothrombosis is a major biological process fostering the pathologies associated with thrombosis.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Reciprocal coupling of coagulation and innate immunity via neutrophil serine proteases.

            Blood neutrophils provide the first line of defense against pathogens but have also been implicated in thrombotic processes. This dual function of neutrophils could reflect an evolutionarily conserved association between blood coagulation and antimicrobial defense, although the molecular determinants and in vivo significance of this association remain unclear. Here we show that major microbicidal effectors of neutrophils, the serine proteases neutrophil elastase and cathepsin G, together with externalized nucleosomes, promote coagulation and intravascular thrombus growth in vivo. The serine proteases and extracellular nucleosomes enhance tissue factor- and factor XII-dependent coagulation in a process involving local proteolysis of the coagulation suppressor tissue factor pathway inhibitor. During systemic infection, activation of coagulation fosters compartmentalization of bacteria in liver microvessels and reduces bacterial invasion into tissue. In the absence of a pathogen challenge, neutrophil-derived serine proteases and nucleosomes can contribute to large-vessel thrombosis, the main trigger of myocardial infarction and stroke. The ability of coagulation to suppress pathogen dissemination indicates that microvessel thrombosis represents a physiological tool of host defense.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment.

              The cytokine macrophage migration inhibitory factor (MIF) plays a critical role in inflammatory diseases and atherogenesis. We identify the chemokine receptors CXCR2 and CXCR4 as functional receptors for MIF. MIF triggered G(alphai)- and integrin-dependent arrest and chemotaxis of monocytes and T cells, rapid integrin activation and calcium influx through CXCR2 or CXCR4. MIF competed with cognate ligands for CXCR4 and CXCR2 binding, and directly bound to CXCR2. CXCR2 and CD74 formed a receptor complex, and monocyte arrest elicited by MIF in inflamed or atherosclerotic arteries involved both CXCR2 and CD74. In vivo, Mif deficiency impaired monocyte adhesion to the arterial wall in atherosclerosis-prone mice, and MIF-induced leukocyte recruitment required Il8rb (which encodes Cxcr2). Blockade of Mif but not of canonical ligands of Cxcr2 or Cxcr4 in mice with advanced atherosclerosis led to plaque regression and reduced monocyte and T-cell content in plaques. By activating both CXCR2 and CXCR4, MIF displays chemokine-like functions and acts as a major regulator of inflammatory cell recruitment and atherogenesis. Targeting MIF in individuals with manifest atherosclerosis can potentially be used to treat this condition.
                Bookmark

                Author and article information

                Contributors
                +65 66015121 , +65 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 October 2016
                14 October 2016
                2016
                : 111
                : 6
                : 69
                Affiliations
                [1 ]Institute of Biochemistry, Medical School, Justus-Liebig University, Giessen, Germany
                [2 ]Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore, 8 College Road, Singapore, 169857 Singapore
                [3 ]National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore
                [4 ]Department of Microbiology, Kazan Federal University, Kazan, Russian Federation
                [5 ]Centro de Biotecnología-FEMSA, Tecnológico de Monterrey, Monterrey, NL Mexico
                [6 ]Research Unit, Hospital of Santa Cristina, Research Institute Princesa, Autonomous University of Madrid, Madrid, Spain
                [7 ]Department of Vascular Biology, Institute for Stroke and Dementia Research, Klinikum der Ludwig-Maximilians-Universität, Munich, Germany
                [8 ]Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
                [9 ]Department of Cardiovascular Surgery, Medical School, Justus-Liebig-University, Giessen, Germany
                [10 ]Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, USA
                [11 ]Department of Cardiology, Aarhus University Hospital, Skejby, Aarhus N, Denmark
                [12 ]Department of Biomedical Sciences, University of Padova, Padua, Italy
                [13 ]Experimental Renal and Cardiovascular Research, Department of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Nuremberg, Germany
                [14 ]Institut für Laboratoriumsmedizin, Ludwig-Maximilians-Universität, Munich, Germany
                [15 ]Institute of Human Genetics, Friedrich-Alexander-Universität Erlangen-Nürnberg, Nuremberg, Germany
                [16 ]Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary
                [17 ]Pharmahungary Group, Szeged, Hungary
                [18 ]Department of Cardiology, Sarawak Heart Centre, Sarawak, Malaysia
                [19 ]Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe-University, Frankfurt, Germany
                [20 ]D. Swarovski Research Lab, Department of Visceral, Transplant Thoracic Surgery, Medical Univ Innsbruck, Innsbruck, Austria
                [21 ]Department of Cardiology, Dong-A University Hospital, Busan, Korea
                [22 ]Hatter Institute and MRC Inter-University Cape Heart Unit, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa
                [23 ]Institute for Molecular Cardiovascular Research, RWTH University Hospital, Aachen, Germany
                [24 ]Department of Cardiology, The Rayne Institute, St Thomas’ Campus, King’s College London, London, UK
                [25 ]The James Black Centre, King’s College, University of London, London, UK
                [26 ]Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
                [27 ]Baker IDI Heart and Diabetes Institute, Melbourne, Australia
                [28 ]Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
                [29 ]Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, UK
                [30 ]Institute of Anatomy and Vascular Biology, Westfalian-Wilhelms-University, Münster, Germany
                [31 ]Institute of Physiology, Justus-Liebig University, Giessen, Germany
                [32 ]Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu, USA
                [33 ]The Hatter Cardiovascular Institute, University College London, London, UK
                [34 ]The National Institute of Health Research University College London Hospitals Biomedical Research Centre, London, UK
                [35 ]Department of Cardiovascular Medicine, National Institute of Cardiology, Ignacio Chavez, Mexico, D.F., Mexico
                Article
                586
                10.1007/s00395-016-0586-x
                5065587
                27743118
                460cc786-203d-43fa-9c79-9736344139ce
                © The Author(s) 2016

                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
                : 14 August 2016
                : 2 October 2016
                : 4 October 2016
                Categories
                Meeting Report
                Custom metadata
                © Springer-Verlag Berlin Heidelberg 2016

                Cardiovascular Medicine
                cardiomyocyte signaling pathways,cardioprotection,cardiovascular disease,co-morbidities,drug targeting,endothelial permeability,extracellular rna (erna),heart regeneration,induced pluripotent stem cells,ischemia–reperfusion injury,lipid metabolism,micrornas (mirnas),mitochondria,remote ischemic conditioning

                Comments

                Comment on this article