한빛사 논문
William Whalen1, Mustafa Buyukozkan2, Bethany Moore3, Jong-Seok Moon4, Charles S Dela Cruz5,6, Fernando J Martinez1, Augustine M K Choi1, Jan Krumsiek2, Heather Stout-Delgado1, Soo Jung Cho1
1Department of Medicine, Pulmonary and Critical Care, Weill Cornell Medicine, New York, New York, USA
2Institute for Computational Biomedicine, Department of Physiology and Biophysics, Weill Cornell Medicine, New York, New York, USA
3Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, USA
4Department of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Asan, Chungcheongnam-do, The Republic of Korea
5Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA
6Pulmonary Critical Care, Yale University School of Medicine, New Haven, Connecticut, USA
Correspondence to Dr Soo Jung Cho
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease with unclear aetiology and poorly understood pathophysiology. Although plasma levels of circulating cell-free DNA (ccf-DNA) and metabolomic changes have been reported in IPF, the associations between ccf-DNA levels and metabolic derangements in lung fibrosis are unclear. Here, we demonstrate that ccf-double-stranded DNA (dsDNA) is increased in patients with IPF with rapid progression of disease compared with slow progressors and healthy controls and that ccf-dsDNA associates with amino acid metabolism, energy metabolism and lipid metabolism pathways in patients with IPF.
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