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      RNase1 as a potential mediator of remote ischaemic preconditioning for cardioprotection†.

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          Abstract

          Remote ischaemic preconditioning (RIPC) is a non-invasive and virtually cost-free strategy for protecting the heart against acute ischaemia-reperfusion injury (IRI). We have recently shown that the inhibition of extracellular RNA (eRNA) using non-toxic RNase1 protected the heart against acute IRI, reduced myocardial infarct (MI) size and preserved left ventricular systolic function in rodent animal MI models. Based on this previous work in animals, the role of the eRNA/RNase1 system in cardiac RIPC in humans should be defined.

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          Author and article information

          Journal
          Eur J Cardiothorac Surg
          European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
          1873-734X
          1010-7940
          Nov 2015
          : 48
          : 5
          Affiliations
          [1 ] Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany Department of Microbiology, Kazan Federal University, Kazan, Russian Federation.
          [2 ] Department of Cardiovascular Surgery, Medical School, Justus-Liebig-University, Giessen, Germany.
          [3 ] Department of Anaesthesia and Intensive Care Medicine, Medical School, Justus-Liebig-University, Giessen, Germany.
          [4 ] Department of Cardiovascular Surgery, Medical School, Justus-Liebig-University, Giessen, Germany andreas.boening@chiru.med.uni-giessen.de.
          Article
          ezu519
          10.1093/ejcts/ezu519
          25564211
          248a850e-08bb-4462-80ee-51229d4f4dbd
          © The Author 2015. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
          History

          Acute inflammation,Cardiac surgery,Extracellular RNA (eRNA),Ischaemia–reperfusion,Remote ischaemic preconditioning,Ribonuclease-1 (RNase1),Tumour necrosis factor-α (TNF-α)

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