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. 2022 Sep 1;27:168. doi: 10.1186/s40001-022-00798-6

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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. 2 — Convergent intracellular signaling in inflammation-related hydrocephalus pathophysiology. Epo erythropoietin, PI3K phosphoinositide 3-kinase, AKT Ak strain transforming kinase / protein kinase B, SGK1 serum- and glucocorticoid-induced kinase 1, WNK with no lysine kinase, TRPV4 transient receptor potential vanilloid 4, NKCC1 sodium potassium 2-chloride cotransporter, NF-kB nuclear factor kappa-light-chain-enhancer of activated B cells, SPAK SPS1-related proline/alanine-rich kinase, TLR4 toll-like receptor 4, TAK1 transforming growth factor beta-activated kinase 1, TGF-β transforming growth factor beta. Figure created in BioRender