Evidence map›Paper›PMID 38212623›Full record

ArticleNature communications2024

In vivo assembly enhanced binding effect augments tumor specific ferroptosis therapy.

Da-Yong Hou, Dong-Bing Cheng, Ni-Yuan Zhang, Zhi-Jia Wang, Xing-Jie Hu, Xin Li, Mei-Yu Lv, Xiang-Peng Li, Ling-Rui Jian, Jin-Peng Ma and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. 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
33.5field-weighted citation impact, top 1% of its field
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, 80 citations in OpenAlex.

  1. Review
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  9. Review
  10. Ferroptosis-centered strategies: redefining therapeutic resistance & adaptation in modern oncology.Apoptosis : an international journal on programmed cell death · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Peptide Multifunctionalization via Modular Construction of Trans-ABAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025
    Review
  19. Review
  20. Article
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

14 authors at 3 institutions in 1 country.

Da-Yong Hou *CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China.ORCID 0000-0002-7567-8663
Dong-Bing Cheng *School of Chemistry, Chemical Engineering & Life Science, Hubei Key Laboratory of Nanomedicine for Neurodegenerative Diseases, Wuhan University of Technology, No. 122 Luoshi Road, Wuhan, 430070, PR China.ORCID 0000-0002-1413-7601
Ni-Yuan Zhang *CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China.
Zhi-Jia WangCAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China.
Xing-Jie HuCAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China.
Xin LiSchool of Chemistry, Chemical Engineering & Life Science, Hubei Key Laboratory of Nanomedicine for Neurodegenerative Diseases, Wuhan University of Technology, No. 122 Luoshi Road, Wuhan, 430070, PR China.
Mei-Yu LvNHC and CAMS Key Laboratory of Molecular Probe and Targeted Theranostics, Harbin Medical University, Harbin, 150001, China.
Xiang-Peng LiCAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China.
Ling-Rui JianNHC and CAMS Key Laboratory of Molecular Probe and Targeted Theranostics, Harbin Medical University, Harbin, 150001, China.
Jin-Peng MaNHC and CAMS Key Laboratory of Molecular Probe and Targeted Theranostics, Harbin Medical University, Harbin, 150001, China.
Taolei SunSchool of Chemistry, Chemical Engineering & Life Science, Hubei Key Laboratory of Nanomedicine for Neurodegenerative Diseases, Wuhan University of Technology, No. 122 Luoshi Road, Wuhan, 430070, PR China. suntl@whut.edu.cn.ORCID 0000-0002-3336-0788
Zeng-Ying QiaoCAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China. qiaozy@nanoctr.cn.ORCID 0000-0002-9932-7702
Wanhai XuNHC and CAMS Key Laboratory of Molecular Probe and Targeted Theranostics, Harbin Medical University, Harbin, 150001, China. xuwanhai@hrbmu.edu.cn.ORCID 0000-0003-3442-7988
Hao WangCAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology (NCNST), Beijing, 100190, China. wanghao@nanoctr.cn.ORCID 0000-0002-1961-0787
Harbin Medical University · CNNational Center for Nanoscience and Technology · CNWuhan University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence indicates that the activation of ferroptosis by glutathione peroxidase 4 (GPX4) inhibitors may be a prominent therapeutic strategy for tumor suppression. However, the wide application of GPX4 inhibitors in tumor therapy is hampered due to poor tumor delivery efficacy and the nonspecific activation of ferroptosis. Taking advantage of in vivo self-assembly, we develop a peptide-ferriporphyrin conjugate with tumor microenvironment specific activation to improve tumor penetration, endocytosis and GPX4 inhibition, ultimately enhancing its anticancer activity via ferroptosis. Briefly, a GPX4 inhibitory peptide is conjugated with an assembled peptide linker decorated with a pH-sensitive moiety and ferriporphyrin to produce the peptide-ferriporphyrin conjugate (Gi-F-CAA). Under the acidic microenvironment of the tumor, the Gi-F-CAA self-assembles into large nanoparticles (Gi-F) due to enhanced hydrophobic interaction after hydrolysis of CAA, improving tumor endocytosis efficiency. Importantly, Gi-F exhibits substantial inhibition of GPX4 activity by assembly enhanced binding (AEB) effect, augmenting the oxidative stress of ferriporphyrin-based Fenton reaction, ultimately enabling antitumor properties in multiple tumor models. Our findings suggest that this peptide-ferriporphyrin conjugate design with AEB effect can improve the therapeutic effect via induction of ferroptosis, providing an alternative strategy for overcoming chemoresistance.

Indexed as

FerroptosisNeoplasmsCell Line, TumorEndocytosisHeminHumansHydrolysisPeptidesTumor MicroenvironmentHeminPeptides

Identifiers

PMID38212623
PMCPMC10784468
OpenAlexW4390751484

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.