Evidence map›Paper›PMID 38685115›Full record

ReviewBiomarker research2024

Disulfidptosis decoded: a journey through cell death mysteries, regulatory networks, disease paradigms and future directions.

Jinyu Chen, Boyuan Ma, Yubiao Yang, Bitao Wang, Jian Hao, Xianhu Zhou

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Biomarker research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
11.1field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
    Pooled it
  2. The emerging roles of disulfidptosis in cancer.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Review
  4. Review
  5. Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Programmed cell death: a promising management for Alzheimer's disease.Apoptosis : an international journal on programmed cell death · 2026
    Review
  14. Article
  15. Review
  16. Ferroptosis-centered strategies: redefining therapeutic resistance & adaptation in modern oncology.Apoptosis : an international journal on programmed cell death · 2026
    Review
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Jinyu ChenThe Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Boyuan MaThe Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Yubiao YangThe Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Bitao WangThe Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Jian HaoThe Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China. haojian@gzhmu.edu.cn.
Xianhu ZhouThe Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China. zhouxianhu@gzhmu.edu.cn.
Guangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

National Natural Science Foundation of China 81371957
6 · The paper itself

Abstract

Cell death is an important part of the life cycle, serving as a foundation for both the orderly development and the maintenance of physiological equilibrium within organisms. This process is fundamental, as it eliminates senescent, impaired, or aberrant cells while also promoting tissue regeneration and immunological responses. A novel paradigm of programmed cell death, known as disulfidptosis, has recently emerged in the scientific circle. Disulfidptosis is defined as the accumulation of cystine by cancer cells with high expression of the solute carrier family 7 member 11 (SLC7A11) during glucose starvation. This accumulation causes extensive disulfide linkages between F-actins, resulting in their contraction and subsequent detachment from the cellular membrane, triggering cellular death. The RAC1-WRC axis is involved in this phenomenon. Disulfidptosis sparked growing interest due to its potential applications in a variety of pathologies, particularly oncology, neurodegenerative disorders, and metabolic anomalies. Nonetheless, the complexities of its regulatory pathways remain elusive, and its precise molecular targets have yet to be definitively identified. This manuscript aims to meticulously dissect the historical evolution, molecular underpinnings, regulatory frameworks, and potential implications of disulfidptosis in various disease contexts, illuminating its promise as a groundbreaking therapeutic pathway and target.

Indexed as

Cystine Cysteine RAC1-WRC pathwayDisulfidptosisFerroptosisGlucose starvationNicotinamide Adenine Dinucleotide Phosphate (NADPH)Pentose phosphate pathway(PPP)SLC7A11

Identifiers

PMID38685115
PMCPMC11059647
OpenAlexW4396217049

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.