Evidence map›Paper›PMID 40258841›Full record

ReviewCell death discovery2025

Targeting epigenetic and post-translational modifications of NRF2: key regulatory factors in disease treatment.

Xinyi Yang, Yingchao Liu, Jinghao Cao, Cuiyun Wu, Lusheng Tang, Wenxia Bian, Yuhan Chen, Lingyan Yu, Yunyi Wu, Sainan Li and 3 more

Abstract readReview
In one paragraph

Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed.

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13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Xinyi Yang *Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Yingchao Liu *Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Jinghao Cao *Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Cuiyun WuCancer Center, Department of Radiology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Lusheng TangLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Wenxia BianLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Yuhan ChenLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Lingyan YuLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Yunyi WuLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Sainan LiLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Yuhuan ShenLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China. shen_yh@zju.edu.cn.
Jun XiaLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China. xiajun@hmc.edu.cn.
Jing DuLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China. dujing1@hmc.edu.cn.ORCID http://orcid.org/0000-0001-7519-8531

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82102938
6 · The paper itself

Abstract

Nuclear factor erythroid 2-related factor 2 (NRF2) is a key transcription factor involved in regulating cellular antioxidant defense and detoxification mechanisms. It mitigates oxidative stress and xenobiotic-induced damage by inducing the expression of cytoprotective enzymes, including HO-1 and NQO1. NRF2 also modulates inflammatory responses by inhibiting pro-inflammatory genes and mediates cell death pathways, including apoptosis and ferroptosis. Targeting NRF2 offers potential therapeutic avenues for treating various diseases. NRF2 is regulated through two principal mechanisms: post-translational modifications (PTMs) and epigenetic alterations. PTMs, including phosphorylation, ubiquitination, and acetylation, play a pivotal role in modulating NRF2's stability, activity, and subcellular localization, thereby precisely controlling its function in the antioxidant response. For instance, ubiquitination can lead to NRF2 degradation and reduced antioxidant activity, while deubiquitination enhances its stability and function. Epigenetic modifications, such as DNA methylation, histone modifications, and interactions with non-coding RNAs (e.g., MALAT1, PVT1, MIR4435-2HG, and TUG1), are essential for regulating NRF2 expression by modulating chromatin architecture and gene accessibility. This paper systematically summarizes the molecular mechanisms by which PTMs and epigenetic alterations regulate NRF2, and elucidates its critical role in cellular defense and disease. By analyzing the impact of PTMs, such as phosphorylation, ubiquitination, and acetylation, as well as DNA methylation, histone modifications, and non-coding RNA interactions on NRF2 stability, activity, and expression, the study reveals the complex cellular protection network mediated by NRF2. Furthermore, the paper explores how these regulatory mechanisms affect NRF2's roles in oxidative stress, inflammation, and cell death, identifying novel therapeutic targets and strategies. This provides new insights into the treatment of NRF2-related diseases, such as cancer, neurodegenerative disorders, and metabolic syndrome. This research deepens our understanding of NRF2's role in cellular homeostasis and lays the foundation for the development of NRF2-targeted therapies.

Identifiers

PMID40258841
PMCPMC12012105

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.