Extract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia of unknown aetiology [1] with ageing being one of the major risk factors [2]. Several ageing-related changes, such as the overproduction of mitochondrial reactive oxygen species, low adenosine triphosphate production, reduced mitochondrial biogenesis and inadequate mitochondrial (mt)DNA repair [3] have also been reported in the IPF lungs [4, 5] and in a bleomycin-induced mouse model [6]. Plasma cell-free DNA, including mtDNA, is released from dying cells into the circulatory system in response to injury [7]. Since circulating mtDNA contains CpG-rich sequences similar to bacterial DNA, disengaged mtDNA can activate the innate immune system by functioning as a damage-associated molecular pattern [8] and contribute to the stimulation of the profibrotic pathway [9].
Abstract
Plasma mtDNA level could serve as a potential marker for disease progression and acute exacerbation in idiopathic pulmonary fibrosis https://bit.ly/2XoXsAv
Acknowledgements
We would like to thank Ye-Jee Kim (Dept of Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea) for their advice on statistical analysis.
Footnotes
Author contributions: Jin Woo Song takes full responsibility for the content of this manuscript, including the data and analyses. Jin Woo Song made substantial contributions to the concept and design of the study. Kwanghun Choi, Miae Kim and Hak-Su Kim performed the experiments. Hee-young Yoon and Jin Woo Song made substantial contributions to the analysis and data interpretation. Hee-young Yoon, Kwanghun Choi and Jin Woo Song drafted the initial manuscript. All authors discussed the results and reviewed the manuscript.
Conflict of interest: Hee-young Yoon has nothing to disclose.
Conflict of interest: Kwanghun Choi has nothing to disclose.
Conflict of interest: Miae Kim has nothing to disclose.
Conflict of interest: Hak-Su Kim has nothing to disclose.
Conflict of interest: Jin Woo Song has nothing to disclose.
Support statement: This work was supported by a grant from the Basic Science Research Program through the National Research Foundation of Korea (NRF), which is funded by the Ministry of Science and Technology (NRF-2019R1A2C2008541), and a grant (2020IL0036) from the Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received March 12, 2020.
- Accepted May 28, 2020.
- Copyright ©ERS 2020
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