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. 2022 Jun 28;29:46. doi: 10.1186/s12929-022-00828-9

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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. 10 — The mechanism for the involvement of the XBP1-Trap1 axis in post-AKI fibrosis. Our results show that AKI induces UPR activation as demonstrated by increased expression of p-PERK, cATF6, and p-IRE1. However, the expression of XBP1 is downregulated and is coincident with decreased expression of Trap1 and elevated expression of α-SMA and fibrosis progression. XBP1 directly regulates Trap1 expression. Restoration of Trap1 expression can alleviate the loss of XBP1 causes prolonged G2/M cell cycle arrest, relieves profibrotic factors expression, and ameliorates renal fibrosis progression