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. 2022 Oct 4;13:492. doi: 10.1186/s13287-022-03181-8

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© The Author(s) 2022

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. 1 — The pathogenetic model of PF. Aging-associated changes, environmental factors and genetic susceptibility result in damage to alveolar epithelial cells. The injured epithelium secretes a plethora of mediators that induce the activation and proliferation of fibroblasts and myofibroblasts, which are resistant to apoptosis and persistently secrete ECM. The ECM also serves as a reservoir of mediators and continuously induces myofibroblast differentiation and ECM secretion in a positive feedback loop, leading to the inexorable progression of PF. By Figdraw (www.figdraw.com)