Evidence map›Paper›PMID 39090114›Full record

ReviewCell death & disease2024

Oxidative cell death in cancer: mechanisms and therapeutic opportunities.

Xiaoqin An, Wenfeng Yu, Jinbao Liu, Daolin Tang, Li Yang, Xin Chen

Abstract readReview
In one paragraph

Review in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 276 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
276citing papers in PubMed, 1 pooled it
–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

276 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
    Pooled it
  2. Article
  3. The role of lysosome-dependent cell death in cancer.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. Anastasis: an unwelcome guest in cancer therapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
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216 more citing papers are in PubMed but not listed here.

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

6 authors.

Xiaoqin AnDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou, PR China.
Wenfeng YuProvincial Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, Guizhou, PR China.
Jinbao LiuGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, PR China.ORCID 0000-0003-2220-2407
Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA. daolin.tang@utsouthwestern.edu.ORCID 0000-0002-1903-6180
Li YangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou, PR China. yangli@gmc.edu.cn.
Xin ChenKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, PR China. chenxin@gzhmu.edu.cn.ORCID 0000-0003-3668-4830

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) are highly reactive oxygen-containing molecules generated as natural byproducts during cellular processes, including metabolism. Under normal conditions, ROS play crucial roles in diverse cellular functions, including cell signaling and immune responses. However, a disturbance in the balance between ROS production and cellular antioxidant defenses can lead to an excessive ROS buildup, causing oxidative stress. This stress damages essential cellular components, including lipids, proteins, and DNA, potentially culminating in oxidative cell death. This form of cell death can take various forms, such as ferroptosis, apoptosis, necroptosis, pyroptosis, paraptosis, parthanatos, and oxeiptosis, each displaying distinct genetic, biochemical, and signaling characteristics. The investigation of oxidative cell death holds promise for the development of pharmacological agents that are used to prevent tumorigenesis or treat established cancer. Specifically, targeting key antioxidant proteins, such as SLC7A11, GCLC, GPX4, TXN, and TXNRD, represents an emerging approach for inducing oxidative cell death in cancer cells. This review provides a comprehensive summary of recent progress, opportunities, and challenges in targeting oxidative cell death for cancer therapy.

Indexed as

Cell DeathNeoplasmsOxidative StressReactive Oxygen SpeciesAnimalsAntioxidantsApoptosisFerroptosisHumansOxidation-ReductionSignal TransductionAntioxidantsReactive Oxygen Species

Identifiers

PMID39090114
PMCPMC11294602

What OpenQuestion holds

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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.