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1532-841422102016OctJournal of cardiac failureJ Card FailLow Circulating Levels of Mitochondrial and High Levels of Nuclear DNA Predict Mortality in Chronic Heart Failure.823828823-810.1016/j.cardfail.2016.06.013S1071-9164(16)30138-5Mitochondrial DNA (mtDNA) and possibly nuclear DNA (nDNA) are released as danger-associated molecular patterns during cardiac stress, and may activate several innate immune receptors. The purpose of this study was to investigate the regulation of these danger-associated molecular patterns during human heart failure (HF).Plasma levels of mtDNA and nDNA from HF patients (n = 84) were analyzed by reverse transcriptase-polymerase chain reaction and compared with controls (n = 72). Increased levels of mtDNA were found in New York Heart Association (NYHA) I-II and NYHA III-IV. There was evidence of increased nDNA in NYHA III-IV compared with controls and NYHA I-II. Kaplan-Meier analysis revealed higher mortality in patients with high nDNA levels, whereas high levels of mtDNA were associated with survival.Plasma levels of mtDNA and nDNA are elevated in human HF associated with increased and decreased mortality, respectively. This study may suggest a rationale for exploring interventions within inflammatory signaling pathways activated by nucleic acids as novel targets in treatment of HF.Copyright © 2016 Elsevier Inc. All rights reserved.DhondupYangchenYResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway. Electronic address: yangched@gmail.com.UelandThorTResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway.DahlChristen PederCPResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.AskevoldErik TandbergETResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway.SandangerØysteinØResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway.FianeArntAFaculty of Medicine, University of Oslo, Norway; Department of Cardiothoracic Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway.OhmIngrid KristineIKResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway.SjaastadIvarICenter for Heart failure Research, University of Oslo, Oslo, Norway; Institute for Experimental Research, Oslo University Hospital, Ullevål, Oslo, Norway.FinsenAlexandra VanessaAVResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway.WæhreAnneACenter for Heart failure Research, University of Oslo, Oslo, Norway; Institute for Experimental Research, Oslo University Hospital, Ullevål, Oslo, Norway.GullestadLarsLCenter for Heart failure Research, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Cardiovascular Research Center, University of Oslo, Oslo, Norway.AukrustPålPResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Rikshospitalet, Oslo, Norway.YndestadArneAResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway.VingeLeif ErikLEResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Internal Medicine, Diakonhjemmet Hospital, Oslo, Norway.engJournal Article20160624
United StatesJ Card Fail94421381071-91640Biomarkers0C1D protein, human0Co-Repressor ProteinsIMAgedBiomarkersbloodCase-Control StudiesCo-Repressor ProteinsmetabolismFemaleHeart FailurebloodmortalityphysiopathologyHumansKaplan-Meier EstimateMaleMiddle AgedMitochondriametabolismPredictive Value of TestsPrognosisReference ValuesSeverity of Illness IndexStatistics, NonparametricSurvival AnalysisDNAinnate immunitymitochondriatoll-like receptor 9
20151022016682016623201662960201662960201711360ppublish2734957110.1016/j.cardfail.2016.06.013S1071-9164(16)30138-5
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