Evidence map›Paper›PMID 39394612›Full record

ReviewCell communication and signaling : CCS2024

Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics.

Tianyi Li, Ying Song, Lijuan Wei, Xiangyi Song, Ruifeng Duan

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

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  18. [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
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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

5 authors.

Tianyi LiDepartment of Cardiology, The Second Hospital of Jilin University, Changchun, Jilin, China.
Ying SongDepartment of Gastroenterology and Digestive Endoscopy Center, The Second Hospital of Jilin University, Chang Chun, Jilin, China.
Lijuan WeiDepartment of Gastroenterology and Digestive Endoscopy Center, The Second Hospital of Jilin University, Chang Chun, Jilin, China.
Xiangyi SongDepartment of Gastroenterology and Digestive Endoscopy Center, The Second Hospital of Jilin University, Chang Chun, Jilin, China.
Ruifeng DuanDepartment of Gastroenterology and Digestive Endoscopy Center, The Second Hospital of Jilin University, Chang Chun, Jilin, China. duanruifeng@jlu.edu.cn.

Funding

Department of Finance of Jilin Province 2019SRCJ012Natural Science Foundation of Jilin Province YDZJ202301ZYTS477
6 · The paper itself

Abstract

Disulfidptosis is a novel discovered form of programmed cell death (PCD) that diverges from apoptosis, necroptosis, ferroptosis, and cuproptosis, stemming from disulfide stress-induced cytoskeletal collapse. In cancer cells exhibiting heightened expression of the solute carrier family 7 member 11 (SLC7A11), excessive cystine importation and reduction will deplete nicotinamide adenine dinucleotide phosphate (NADPH) under glucose deprivation, followed by an increase in intracellular disulfide stress and aberrant disulfide bond formation within actin networks, ultimately culminating in cytoskeletal collapse and disulfidptosis. Disulfidptosis involves crucial physiological processes in eukaryotic cells, such as cystine and glucose uptake, NADPH metabolism, and actin dynamics. The Rac1-WRC pathway-mediated actin polymerization is also implicated in this cell death due to its contribution to disulfide bond formation. However, the precise mechanisms underlying disulfidptosis and its role in tumors are not well understood. This is probably due to the multifaceted functionalities of SLC7A11 within cells and the complexities of the downstream pathways driving disulfidptosis. This review describes the critical roles of SLC7A11 in cells and summarizes recent research advancements in the potential pathways of disulfidptosis. Moreover, the less-studied aspects of this newly discovered cell death process are highlighted to stimulate further investigations in this field.

Indexed as

Actin CytoskeletonNeoplasmsAmino Acid Transport System y+AnimalsCell DeathHumansAmino Acid Transport System y+SLC7A11 protein, humanActin dynamicsArp2/3 complexCancer treatmentCystineDisulfide stressDisulfidptosisProgrammed cell deathRac1SLC7A11WAVE regulatory complex

Identifiers

PMID39394612
PMCPMC11470700

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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.