Evidence map›Paper›PMID 40285867›Full record

ReviewCell biology and toxicology2025

Lipotoxicity, lipid peroxidation and ferroptosis: a dilemma in cancer therapy.

Chuhan Ma, Huixin Hu, Hao Liu, Chongli Zhong, Baokang Wu, Chao Lv, Yu Tian

Abstract readReview
In one paragraph

Review in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Review
  2. Review
  3. Targeting ferroptosis to overcome drug resistance in gastrointestinal cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  4. Review
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  8. Review
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  10. Review
  11. Article
  12. 4-Hydroxynonenal, a Potential Biomarker for Lung Inflammatory Diseases.International journal of molecular sciences · 2026
    Review
  13. Review
  14. Article
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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

7 authors.

Chuhan MaDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China.
Huixin HuDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China.
Hao LiuDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China.
Chongli ZhongDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China.
Baokang WuDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China.
Chao Lv *Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China. clu@cmu.edu.cn.
Yu Tian *Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning Province, China. yu.tian@cmu.edu.cn.

Funding

National Natural Science Foundation of China 81974377
6 · The paper itself

Abstract

The vulnerability of tumor cells to lipid peroxidation, driven by redox imbalance and lipid overabundance within the tumor microenvironment (TME), has become a focal point for novel antitumor strategies. Ferroptosis, a form of regulated cell death predicated on lipid peroxidation, is emerging as a promising approach. Beyond their role in directly eliminating tumor cells, lipid peroxidation and its products, such as 4-hydroxynonenal (HNE), exert an additional influence by damaging DNA and shaping an environment conducive to tumor growth and metastasis. This process polarizes macrophages towards a pro-inflammatory phenotype, dampens the antigen-presenting capacity of dendritic cells (DCs), and undermines the cytotoxic functions of T and NK cells. Furthermore, it transforms neutrophils into pro-tumorigenic polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). The lipid peroxidation of stroma cells also contributes to tumor progression. Although advanced nanotherapies have shown the ability to target tumor cells precisely, they often overlook the nuanced effects of lipid peroxidation products. In this review, we highlight a synergistic mechanism in which lipid peroxidation products and ferroptosis contribute to an immunosuppressive state that is temporally distinct from cell death. This insight broadens our understanding of ferroptosis-derived immunosuppression, encompassing all types of immune cells within the TME. This review aims to catalyze further research in this underexplored area, emphasizing the potential of lipid peroxidation products to hinder the clinical translation of ferroptosis-based therapies.

Indexed as

FerroptosisLipid PeroxidationNeoplasmsAldehydesAnimalsHumansTumor Microenvironment4-hydroxy-2-nonenalAldehydesActive aldehydeFerroptosisImmune cellsLipid peroxidationOxidized lipid

Identifiers

PMID40285867
PMCPMC12033115

What OpenQuestion holds

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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.