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Global Translational Medicine Risk factors of idiopathic pulmonary fibrosis

lung fibrosis. We are currently in the process of lncRNA References
extraction and studying their expression profile in 1. Wynn TA, Ramalingam TR, 2012, Mechanisms of fibrosis:
peripheral blood leukocytes and lung tissue for further Therapeutic translation for fibrotic disease. Nat Med,
comparison with clinical parameters. The study of 18: 1028–1040.
lncRNA-mediated mechanisms of fibrosis development https://doi.org/10.1038/nm.2807
is an important and urgent task, since many lncRNAs,
including those we have studied, are potential disease 2. Rockey DC, Bell PD, Hill JA, 2015, Fibrosis a common
biomarkers and targets for specific pharmacological pathway to organ injury and failure. N Engl J Med, 372:
therapy. In addition, they can serve as diagnostic and 1138–1149.
prognostic targets for early detection and prediction of the https://doi.org/10.1056/NEJMra1300575
course of idiopathic and COVID-19-induced pulmonary 3. Zhao X, Sun J, Chen Y, et al., 2018, LncRNA PFAR promotes
fibrosis. lung fibroblast activation and fibrosis by targeting miR-138
to regulate the YAP1-twist axis. Mol Ther, 26: 2206–2217.
Acknowledgments https://doi.org/10.1016/j.ymthe.2018.06.020

We acknowledge Zuhra M. Zaynullina for her kind 4. Yan W, Wu Q, Yao W, et al., 2017, MiR-503 modulates
assistance. epithelial-mesenchymal transition in silica-induced
pulmonary fibrosis by targeting PI3K p85 and is sponged by
Funding lncRNA MALAT1. Sci Rep, 7: 11313.
The study was performed under the support of grant of https://doi.org/10.1038/s41598-017-11904-8
Russian Scientific Foundation 22-25-00019, http://rscf.ru/ 5. Richeldi L, Collard HR, Jones MG, 2017, Idiopathic
project/22-25-00019. pulmonary fibrosis. Lancet, 389:1941–1952.

Conflict of interest https://doi.org/10.1016/S0140-6736(17)30866-8
6. Lederer DJ, Martinez FJ, 2018, Idiopathic pulmonary
None of the authors has conflicts of interest to report with fibrosis. N Engl J Med, 378: 1811–1823.
regard to this manuscript.
https://doi.org/10.1056/NEJMra1705751
Author contributions 7. Martinez FJ, Collard HR, Pardo A, et al., 2017, Idiopathic

Conceptualization: Rustem H. Zulkarneev, Gulnaz pulmonary fibrosis. Nat Rev Dis Primers, 3: 17074.
Faritovna Korytina, Naufal Shamilevich Zagidullin https://doi.org/10.1038/nrdp.2017.74
Funding acquisition: Gulnaz Faritovna Korytina, Naufal 8. Hirahara K, Aoki A, Morimoto Y, et al., 2019, The
Shamilevich Zagidullin immunopathology of lung fibrosis: Amphiregulin-
Project administration: Naufal Shamilevich Zagidullin producing pathogenic memory T helper-2 cells control the
Writing – original draft: Shamil R. Zulkarneev, Rustem H. airway fibrotic responses by inducing eosinophils to secrete
Zulkarneev, Gulnaz Faritovna Korytina, Irshat A. osteopontin. Semin Immunopathol, 41: 339–348.
Gibadullin, Arthur M. Avzaletdinov, Zhihui Niu, https://doi.org/10.1007/s00281-019-00735-6
Jiayu Guo, Yulia Genadievna Aznabaeva, Guzel M. 9. Henderson NC, Rieder F, Wynn TA, 2020, Fibrosis: From
Nurtdinova, Naufal Shamilevich Zagidullin mechanisms to medicines. Nature, 587: 555–566.
Writing – review & editing: Shamil R. Zulkarneev, https://doi.org/10.1038/s41586-020-2938-9
Rustem H. Zulkarneev, Gulnaz Faritovna Korytina,
Naufal Shamilevich Zagidullin. 10. Chanda D, Otoupalova E, Smith SR, et al., 2019,
Developmental pathways in the pathogenesis of lung
Ethics approval and consent to participate fibrosis. Mol Aspects Med, 65: 56–69.
Not applicable. https://doi.org/10.1016/j.mam.2018.08.004
Consent for publication 11. Zhu L, Fu X, Chen X, et al., 2017, M2 macrophages induce
EMT through the TGF-β/Smad2 signaling pathway. Cell
Not applicable. Biol Int, 41: 960–968.
https://doi.org/10.1002/cbin.10788
Availability of data
12. Kugler MC, Joyner AL, Loomis CA, et al., 2015, Sonic
Not applicable. hedgehog signaling in the lung. From development to

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