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. 2023 Jan 19;20:2. doi: 10.1186/s12950-023-00329-y

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — NETs drive lung epithelial injury and pulmonary fibrosis. MPO, DNA and histones in Nets can cause damage to alveolar epithelial cells, which release a large number of pro-inflammatory and pro-fibrotic factors (including IL-6, IL-8, IL-1α, IL-1β and TNF-α) and initiate subsequent inflammatory immune repair. Excessive repair of alveolar epithelial cells after injury is an important mechanism of pulmonary fibrosis. HMGB1 in NETs could act on the RAGE receptors in lung epithelial cells, which in turn leads to the downregulation of the epithelial cell marker E-cadherin and the upregulation of the myofibroblast cell marker α-SMA. NETs: neutrophil extracellular traps; MPO: myeloperoxidase; HMGB1: high mobility group box 1; RAGE: the receptor of advanced glycation end-product; α-SMA: alpha-smooth muscle actin