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. 2022 Feb 18;12:18. doi: 10.1186/s13578-022-00747-0

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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 — Mechanism of UPR^mt in mammals. Upon ROS accumulation in IMS, the AKT-ERα axis is activated to trigger the transcription of NRF1 and HTRA2 in response to IMS damage. When ATF5 senses mitochondrial disorders, it translocates to the nucleus together with ATF4 and CHOP to synergistically promote the expression of mitochondrial chaperones and proteases. HSF1 forms a complex with SSBP1 and recruits the chromatin remodeling factor BRG1, consequently inducing the expression of mtHSPs. The SIRT3-FOXO3 axis is involved in antioxidant stress and mitophagy. The interaction of NRF1 and SIRT7 inhibits mitochondrial respiration and biogenesis, thereby reducing the load of damaged proteins. In summary, the mammalian UPR^mt promotes mitochondrial recovery and maintains proteostasis through a variety of pathways