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. 2023 Feb 23;20:45. doi: 10.1186/s12974-023-02731-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. 8 — Retina–bone-marrow–blood–retina pathway of fibrocytes and macrophage recruitment in the development of subretinal fibrosis. Retinal injury is detected by the bone marrow, which then produces fibrocytes and pro-fibrotic macrophages and releases them to the blood circulation. Once recruited into the damaged site, fibrocytes can differentiate into myofibroblasts. Macrophages can release profibrotic factors that promote epithelial-to-mesenchymal transition (EMT) in RPE cells. Macrophages can also participate in subretinal fibrosis through macrophage-to-myofibroblast transition (MMT). This process is augmented during ageing. (Image was created in BioRender.com)