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. 2024 Aug 30;12:92. doi: 10.1186/s40364-024-00641-6

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© The Author(s) 2024

Open Access This 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. 5 — Mechanisms of pulmonary fibrosis involved in BRD4 and anti-pulmonary fibrosis effects and the mechanisms of BRD4 inhibitors. BRD4 is involved in fibrotic phenotypic changes in lung fibroblasts (LFs) and epithelial cells caused by external stimuli. It mainly affects the expression of fibrosis-related genes. BRD4 inhibitors (JQ1, ZL0591, CG233, OTX015, and ARV-825) exert their anti-pulmonary fibrosis effects mainly through the inhibition of BRD4-mediated gene transcription, the activation of LFs, the EMT process and oxidative stress