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Low Circulating Levels of Mitochondrial and High Levels of Nuclear DNA Predict Mortality in Chronic Heart Failure.
Dhondup, Yangchen; Ueland, Thor; Dahl, Christen Peder; Askevold, Erik Tandberg; Sandanger, Øystein; Fiane, Arnt; Ohm, Ingrid Kristine; Sjaastad, Ivar; Finsen, Alexandra Vanessa; Wæhre, Anne; Gullestad, Lars; Aukrust, Pål; Yndestad, Arne; Vinge, Leif Erik.
Affiliation
  • Dhondup Y; Research 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. Electroni
  • Ueland T; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway.
  • Dahl CP; Research 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.
  • Askevold ET; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Heart failure Research, University of Oslo, Oslo, Norway.
  • Sandanger Ø; Research 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.
  • Fiane A; Faculty of Medicine, University of Oslo, Norway; Department of Cardiothoracic Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway.
  • Ohm IK; Research 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.
  • Sjaastad I; Center for Heart failure Research, University of Oslo, Oslo, Norway; Institute for Experimental Research, Oslo University Hospital, Ullevål, Oslo, Norway.
  • Finsen AV; Research 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.
  • Wæhre A; Center for Heart failure Research, University of Oslo, Oslo, Norway; Institute for Experimental Research, Oslo University Hospital, Ullevål, Oslo, Norway.
  • Gullestad L; Center 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.
  • Aukrust P; Research 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 Hospit
  • Yndestad A; Research 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.
  • Vinge LE; Research 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 Hospi
J Card Fail ; 22(10): 823-8, 2016 Oct.
Article in En | MEDLINE | ID: mdl-27349571
ABSTRACT

BACKGROUND:

Mitochondrial 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). METHODS AND

RESULTS:

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.

CONCLUSIONS:

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.
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Full text: 1 Database: MEDLINE Main subject: Co-Repressor Proteins / Heart Failure / Mitochondria Type of study: Observational_studies / Prognostic_studies / Risk_factors_studies Limits: Aged / Female / Humans / Male / Middle aged Language: En Year: 2016 Type: Article
Fulltext
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Full text: 1 Database: MEDLINE Main subject: Co-Repressor Proteins / Heart Failure / Mitochondria Type of study: Observational_studies / Prognostic_studies / Risk_factors_studies Limits: Aged / Female / Humans / Male / Middle aged Language: En Year: 2016 Type: Article