Evidence map›Paper›PMID 40419525›Full record

ArticleNature communications2025

Provoking tumor disulfidptosis by single-atom nanozyme via regulating cellular energy supply and reducing power.

Wenxin Yu, Duo Jin, Yajie Zhang, Shenghu Wang, Jiaji Yu, Manman Liu, Yi Dai, Yichen Yin, Junjie Cheng, Yangzhong Liu

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. An In Situ HAdvanced materials (Deerfield Beach, Fla.) · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. [Exploring the protective effects and mechanisms of HYX1-derived exosomes on acute liver failure based on disulfidptosis signaling].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. 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

10 authors.

Wenxin Yu *Department of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China.ORCID http://orcid.org/0000-0003-0051-0185
Duo Jin *Department of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China.ORCID http://orcid.org/0000-0002-0949-3310
Yajie ZhangCentral Laboratory, Department of Biobank, Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0003-2510-6015
Shenghu WangDepartment of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China.ORCID http://orcid.org/0009-0009-3516-9838
Jiaji YuDepartment of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China.
Manman LiuDepartment of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China.
Yi DaiCollege of Pharmaceutical Sciences, Anhui Xinhua University, Hefei, China.ORCID http://orcid.org/0009-0005-8814-3165
Yichen YinDepartment of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China.ORCID http://orcid.org/0009-0001-5434-1869
Junjie ChengDepartment of Radiology, Zhongda Hospital, Medical School; Department of Nutrition and Food Hygiene, School of Public Health, Southeast University, Nanjing, China. jjcheng@ustc.edu.cn.ORCID http://orcid.org/0000-0003-0502-6712
Yangzhong LiuDepartment of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparations and Clinical Pharmacy, University of Science and Technology of China, Hefei, China. liuyz@ustc.edu.cn.ORCID http://orcid.org/0000-0003-2891-7964

Funding

National Natural Science Foundation of China (National Science Foundation of China) 52021002, 32101121, 22377116, 22177109
6 · The paper itself

Abstract

Disulfidptosis, a recently identified form of programmed cell death, is initiated by depletion of endogenous nicotinamide adenine dinucleotide phosphate (NADPH) under glucose starvation. Tumor cells, owing to their heightened requirements of energy and nutrients, are more susceptible to disulfidptosis than normal cells. Here, we introduced an effective strategy to induce tumor disulfidptosis via interrupting cellular energy supply and reducing power by integrating a copper single-atom nanozyme (CuSAE) and glucose oxidase (GOx). GOx induces glucose starvation, impeding generation of NADPH through pentose phosphate pathway (PPP). CuSAE mimics NADPH oxidase, depleting existing NADPH, which intensifies the blockade of disulfide reduction and efficiently triggers disulfidptosis of tumor cells. Furthermore, CuSAE exhibits peroxidase- and glutathione oxidase-mimicking activities, catalyzing generation of •OH radical and depletion cellular GSH, which enhances oxidative stress and exacerbates cell damage. Disulfidptosis is confirmed as the predominant type of cell death induced by GOx/CuSAE. In vivo assays demonstrated the high antitumor potency of GOx/CuSAE in treating with female tumor-bearing mice, with minimal systemic toxicity observed. This work introduces a promising strategy for designing antitumor agents by inducing disulfidptosis. The enzyme hybrids that combine nanozymes and natural enzymes offer a feasible approach to achieve this multifaceted therapeutic goal.

Indexed as

Antineoplastic AgentsApoptosisCopperNeoplasmsAnimalsCell Line, TumorDisulfidptosisEnergy MetabolismFemaleGlucoseGlucose OxidaseGlutathioneHumansMiceNADPOxidation-ReductionAntineoplastic AgentsCopperGlucoseGlucose OxidaseGlutathioneNADP

Identifiers

PMID40419525
PMCPMC12106855

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.