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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. 1 — Schematic diagram of the mechanism of organ fibrosis. When tissues and organs such as the heart, liver, lung and kidney are subjected to sustained external injury, damaged parenchymal cells initiate injury-related molecular patterns, secrete inflammatory mediators, recruit inflammatory cells, and promote inflammation in damaged tissues. Quiescent fibroblasts in these organs are activated to become myofibroblasts in response to the body's repair response to damaged tissues, and epithelial-mesenchymal transition (EMT) and endothelial-mesenchymal transition (EndMT) further increase the number of myofibroblasts in damaged organs. Myofibroblasts continuously secrete extracellular matrix (ECM), such as α-smooth muscle actin (α-SMA), collagen I (COL I), and fibronectin (FN), which leads to the development of organ fibrosis [7, 67–70]