Evidence map›Paper›PMID 39354653›Full record

ReviewCell proliferation2025

Mechanisms and therapeutic potential of disulphidptosis in cancer.

Yanhu Li, Haijun Zhang, Fengguang Yang, Daxue Zhu, Shijie Chen, Zhaoheng Wang, Ziyan Wei, Zhili Yang, Jingwen Jia, Yizhi Zhang and 3 more

Abstract readReview
In one paragraph

Review in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
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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.

Yanhu LiLanzhou University Second Hospital, Lanzhou, PR China.ORCID https://orcid.org/0009-0002-4512-0818
Haijun ZhangLanzhou University Second Hospital, Lanzhou, PR China.
Fengguang YangLanzhou University Second Hospital, Lanzhou, PR China.ORCID https://orcid.org/0000-0002-4384-8306
Daxue ZhuLanzhou University Second Hospital, Lanzhou, PR China.ORCID https://orcid.org/0000-0002-8418-9757
Shijie ChenLanzhou University Second Hospital, Lanzhou, PR China.
Zhaoheng WangLanzhou University Second Hospital, Lanzhou, PR China.
Ziyan WeiLanzhou University Second Hospital, Lanzhou, PR China.
Zhili YangLanzhou University Second Hospital, Lanzhou, PR China.
Jingwen JiaLanzhou University Second Hospital, Lanzhou, PR China.
Yizhi ZhangLanzhou University Second Hospital, Lanzhou, PR China.ORCID https://orcid.org/0009-0004-1775-3612
Dongxin WangLanzhou University Second Hospital, Lanzhou, PR China.
Mingdong MaLanzhou University Second Hospital, Lanzhou, PR China.
Xuewen KangLanzhou University Second Hospital, Lanzhou, PR China.ORCID https://orcid.org/0000-0002-5877-9198

Funding

National Natural Science Foundation of China 82272536Natural Science Foundation of Gansu Province 24JRRA1158
6 · The paper itself

Abstract

SLC7A11 plays a pivotal role in tumour development by facilitating cystine import to enhance glutathione synthesis and counteract oxidative stress. Disulphidptosis, an emerging form of cell death observed in cells with high expression of SLC7A11 under glucose deprivation, is regulated through reduction-oxidation reactions and disulphide bond formation. This process leads to contraction and collapse of the F-actin cytoskeleton from the plasma membrane, ultimately resulting in cellular demise. Compared to other forms of cell death, disulphidptosis exhibits distinctive characteristics and regulatory mechanisms. This mechanism provides novel insights and innovative strategies for cancer treatment while also inspiring potential therapeutic approaches for other diseases. Our review focuses on elucidating the molecular mechanism underlying disulphidptosis and its connection with the actin cytoskeleton, identifying alternative metabolic forms of cell death, as well as offering insights into disulphidptosis-based cancer therapy. A comprehensive understanding of disulphidptosis will contribute to our knowledge about fundamental cellular homeostasis and facilitate the development of groundbreaking therapies for disease treatment.

Indexed as

NeoplasmsActin CytoskeletonAmino Acid Transport System y+AnimalsCell DeathHumansOxidative StressAmino Acid Transport System y+SLC7A11 protein, human

Identifiers

PMID39354653
PMCPMC11693557

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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.