Evidence map›Paper›PMID 42177709›Full record

ReviewApoptosis : an international journal on programmed cell death2026

Disulfidptosis in hepatocellular carcinoma: molecular mechanisms, therapeutic potential, and exploratory insights into chronic liver diseases.

Yuting Liu, Wenzhuo Hu, Jingyin Mai, Yang Cheng

Abstract readReview
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In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Yuting Liu *Institute of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Wenzhuo Hu *The First Rehabilitation Hospital of Shanghai, Shanghai, China.
Jingyin MaiDepartment of Emergency and Critical Care Medicine, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. maijingyin@126.com.
Yang ChengInstitute of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China. drchengyang@126.com.

Funding

National Natural Science Foundation of China (No. 82374189). No. 82374189
6 · The paper itself

Abstract

Disulfidptosis, a newly identified form of programmed cell death (PCD) that was discovered in 2023, occurs specifically in cells with high SLC7A11 expression when glucose is scarce. The underlying mechanism involves NADPH depletion, which triggers severe disulfide stress and ultimately causes the actin cytoskeleton to collapse. In recent years, researchers have increasingly focused on the potential role of disulfidptosis in liver diseases. Current evidence mainly supports its involvement in hepatocellular carcinoma (HCC), with some preliminary data also suggesting connections to liver cirrhosis and metabolic liver disorders. This review critically synthesizes the molecular mechanisms underlying disulfidptosis, explores its possible links to various liver conditions based on the available evidence, and assesses the potential of disulfidptosis-related genes (DRGs) as exploratory tools for diagnosis, prognostic stratification, and exploratory therapeutic prediction. Together, these insights provide a foundation for understanding liver disease pathogenesis and may guide future research efforts, pending rigorous experimental and clinical validation.

Indexed as

Carcinoma, HepatocellularDisulfidptosisLiver DiseasesLiver NeoplasmsAmino Acid Transport System y+AnimalsHumansNADPAmino Acid Transport System y+NADPSLC7A11 protein, humanDisulfide stressDisulfidptosisHCCNADPHSLC7A11

Identifiers

What OpenQuestion holds

Textmetadata
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.