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. 2024 Mar 9;98(5):1399–1413. doi: 10.1007/s00204-024-03700-x

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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/.

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Fig. 8 — Diagram of the mechanism by which circMKLN1 promotes pulmonary fibrosis. The expression of circMKLN1 was increased in pulmonary fibrosis and promoted the EMT of AECs. The mechanism of circMKLN1 in this process might involve sponging miR-26a/b and upregulating CDK8