Evidence map›Paper›PMID 41826762›Full record

ArticleNature chemical biology2026

IDO1 regulating ROS rhythm reveals glycogenolysis/PPP as a cancer treatment target.

Nannan Zhou, Zheng Ling, Xiankai Cao, Chaoqi Zhang, Dianheng Wang, Chaoying Zhang, Lu Zhang, Dingfei Yan, Jie Chen, Yabo Zhou and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature chemical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

17 authors.

Nannan Zhou *Department of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Zheng Ling *Department of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xiankai Cao *Department of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Chaoqi Zhang *Department of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Dianheng WangDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Chaoying ZhangDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Lu ZhangTianjin Centers for Disease Control and Prevention, Tianjin, China.
Dingfei YanMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing, China.
Jie ChenDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yabo ZhouDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Li ZhouDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Zhenfeng WangDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jingwei MaDepartment of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ke TangDepartment of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huafeng ZhangDepartment of Pathology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jiadi LvDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Bo HuangDepartment of Immunology and National Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. tjhuangbo@hotmail.com.ORCID http://orcid.org/0000-0001-8476-1138

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) dynamics exhibits rhythmic oscillations in cancer cells but how this rhythm influences tumorigenesis and therapeutic responses remains unclear. Here we found coexistence of ROS rhythmicity and rhythm loss in tumor samples. Under low-ROS conditions, indoleamine 2,3-dioxygenase 1 (IDO1), an immune-checkpoint molecule, binds to KEAP1 for proteasomal degradation in the nucleus. In contrast, elevated ROS levels drive IDO1 translocation into the cytosol, where it binds mitochondria-released heme to form an active holoenzyme. This holoenzyme catalyzes tryptophan to kynurenine that allosterically activates glucose-6-phosphate dehydrogenase, enhancing NADPH production and promoting ROS clearance. However, in hypoxic tumor microenvironments, ROS rhythmicity is lost. Compensating for this, hypoxic tumor cells mobilize the sulfenylated aryl hydrocarbon receptor (AhR)-mediated glycogenolysis pathway to manage disordered ROS accumulation, maintaining elevated ROS levels that favor tumor growth. Dual inhibition of IDO1 and AhR significantly prolongs survival of NSG mice, highlighting enforced disruption of ROS rhythm as a common therapeutic strategy.

Indexed as

GlycogenolysisIndoleamine-Pyrrole 2,3,-DioxygenaseNeoplasmsPentose Phosphate PathwayReactive Oxygen SpeciesAnimalsCell Line, TumorHumansKelch-Like ECH-Associated Protein 1MiceReceptors, Aryl HydrocarbonTumor MicroenvironmentIDO1 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Reactive Oxygen SpeciesReceptors, Aryl Hydrocarbon

Identifiers

PMID41826762

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.