SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury

Abstract NRF2 has been recognized as a central hub that neutralizes ROS and restores intracellular redox balance. In addition to KEAP1 mediated ubiquitin-proteasome degradation, post-translational modifications of NRF2 are critical for regulating its nuclear translocation and activation but precise...

Full description

Saved in:
Bibliographic Details
Main Authors: Tingzi Yu, Cong Ding, Jinying Peng, Gaoshuang Liang, Yongyi Tang, Jinqiu Zhao, Zhuan Li
Format: Article
Language:English
Published: Nature Publishing Group 2025-04-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-025-07549-5
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850258502794084352
author Tingzi Yu
Cong Ding
Jinying Peng
Gaoshuang Liang
Yongyi Tang
Jinqiu Zhao
Zhuan Li
author_facet Tingzi Yu
Cong Ding
Jinying Peng
Gaoshuang Liang
Yongyi Tang
Jinqiu Zhao
Zhuan Li
author_sort Tingzi Yu
collection DOAJ
description Abstract NRF2 has been recognized as a central hub that neutralizes ROS and restores intracellular redox balance. In addition to KEAP1 mediated ubiquitin-proteasome degradation, post-translational modifications of NRF2 are critical for regulating its nuclear translocation and activation but precise mechanisms underly this regulation remain elusive. In this study, we found that SIRT7 was sufficient and essential for NRF2 nuclear localization and activation. Knockdown of SIRT7 significantly impaired intercellular ROS homeostasis and increased apoptosis in response to oxidative stress including chemodrug treatment. SIRT7 interacted with NRF2 and induced its deacetylation, by which inhibited binding of NRF2 to KEAP1, enhanced NRF2 protein stability and promoted its nuclear translocation. SIRT7 induced NRF2 deacetylation at K443 and K518 sites. Lysine-arginine mutations of these sites (2KR NRF2) significantly reduced KEAP1/NRF2 binding, increased NRF2 nuclear translocation and target gene expression, decreased intercellular ROS level, whereas lysine-glutamine (2KQ) mutant showed similar subcellular localization and functions with WT. Knockdown SIRT7 in hepatocyte exacerbated Oxaliplatin (Oxa) induced hepatic injury and inflammation. While AAV8-NRF2-mediated hepatic NRF2 overexpression or NRF2 agonist significantly prevented Oxa-induced elevation of ALT levels, sinusoidal dilatation and inflammation in SIRT7 HKO mice. Our data thus uncovered previously unidentified role of SIRT7 in modulating NRF2 nuclear localization and activation via deacetylation. Activating SIRT7 might offer protection against chemodrug-induced liver injury.
format Article
id doaj-art-2d045ceb9bd94b9b80a35497a63a484c
institution OA Journals
issn 2041-4889
language English
publishDate 2025-04-01
publisher Nature Publishing Group
record_format Article
series Cell Death and Disease
spelling doaj-art-2d045ceb9bd94b9b80a35497a63a484c2025-08-20T01:56:09ZengNature Publishing GroupCell Death and Disease2041-48892025-04-0116111510.1038/s41419-025-07549-5SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injuryTingzi Yu0Cong Ding1Jinying Peng2Gaoshuang Liang3Yongyi Tang4Jinqiu Zhao5Zhuan Li6The Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical ScienceThe Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical ScienceThe Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical ScienceThe Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical ScienceThe Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical ScienceDepartment of infectious disease, The First Affiliated Hospital of Chongqing Medical UniversityThe Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical ScienceAbstract NRF2 has been recognized as a central hub that neutralizes ROS and restores intracellular redox balance. In addition to KEAP1 mediated ubiquitin-proteasome degradation, post-translational modifications of NRF2 are critical for regulating its nuclear translocation and activation but precise mechanisms underly this regulation remain elusive. In this study, we found that SIRT7 was sufficient and essential for NRF2 nuclear localization and activation. Knockdown of SIRT7 significantly impaired intercellular ROS homeostasis and increased apoptosis in response to oxidative stress including chemodrug treatment. SIRT7 interacted with NRF2 and induced its deacetylation, by which inhibited binding of NRF2 to KEAP1, enhanced NRF2 protein stability and promoted its nuclear translocation. SIRT7 induced NRF2 deacetylation at K443 and K518 sites. Lysine-arginine mutations of these sites (2KR NRF2) significantly reduced KEAP1/NRF2 binding, increased NRF2 nuclear translocation and target gene expression, decreased intercellular ROS level, whereas lysine-glutamine (2KQ) mutant showed similar subcellular localization and functions with WT. Knockdown SIRT7 in hepatocyte exacerbated Oxaliplatin (Oxa) induced hepatic injury and inflammation. While AAV8-NRF2-mediated hepatic NRF2 overexpression or NRF2 agonist significantly prevented Oxa-induced elevation of ALT levels, sinusoidal dilatation and inflammation in SIRT7 HKO mice. Our data thus uncovered previously unidentified role of SIRT7 in modulating NRF2 nuclear localization and activation via deacetylation. Activating SIRT7 might offer protection against chemodrug-induced liver injury.https://doi.org/10.1038/s41419-025-07549-5
spellingShingle Tingzi Yu
Cong Ding
Jinying Peng
Gaoshuang Liang
Yongyi Tang
Jinqiu Zhao
Zhuan Li
SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury
Cell Death and Disease
title SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury
title_full SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury
title_fullStr SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury
title_full_unstemmed SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury
title_short SIRT7-mediated NRF2 deacetylation promotes antioxidant response and protects against chemodrug-induced liver injury
title_sort sirt7 mediated nrf2 deacetylation promotes antioxidant response and protects against chemodrug induced liver injury
url https://doi.org/10.1038/s41419-025-07549-5
work_keys_str_mv AT tingziyu sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury
AT congding sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury
AT jinyingpeng sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury
AT gaoshuangliang sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury
AT yongyitang sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury
AT jinqiuzhao sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury
AT zhuanli sirt7mediatednrf2deacetylationpromotesantioxidantresponseandprotectsagainstchemodruginducedliverinjury