Evidence map›Paper›PMID 42163887›Full record

ReviewAmerican journal of cancer research2026

The ferroptosis-tumor microenvironment nexus: bidirectional regulation in cancer pathogenesis and therapeutic opportunities.

Lin-Jiu Wu, Xiao-Qing Liu

Abstract readReview
In one paragraph

Review in American journal of cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

2 authors.

Lin-Jiu WuNanchang People's Hospital Affiliated to Nanchang Medical College Nanchang, Jiangxi, China.
Xiao-Qing LiuNanchang People's Hospital Affiliated to Nanchang Medical College Nanchang, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review systematically dissects the mechanisms of the bidirectional ferroptosis-tumor microenvironment (TME) regulation. The TME modulates ferroptosis susceptibility in immune cells through metabolic reprogramming and transcriptional regulation, while immune cells induce tumor cells ferroptosis via cytokine signaling and redox disruption. Intercellular crosstalk among immune and stromal cells further shapes ferroptotic responses through multidimensional mechanisms, forming a complex regulatory network. Paradoxically, ferroptosis exerts dual effects on the TME: it enhances antitumor immunity via damage-associated molecular patterns (DAMPs)-mediated dendritic cells (DCs) activation and T cell priming, yet promotes immune evasion through immunosuppressive niche formation and checkpoint upregulation. Current therapeutic strategies focus on glutathione peroxidase 4 (GPX4) inhibitors, synergistic combinations with immune checkpoint inhibitor (ICI), and nanotechnology-enabled targeted delivery systems. Persistent challenges include tumor heterogeneity, off-target toxicity, and deficiency in pharmacokinetics. Future research should prioritize two strategies: ferroptosis biomarker-guided patient stratification and TME-responsive smart drug delivery systems, optimizing personalized therapies to improve survival outcomes. By elucidating the ferroptosis-TME nexus, this review provides novel insights for advancing precision oncology and immunotherapeutic paradigms.

Indexed as

cancer therapyCD8+ T cellFerroptosisimmunotherapylipid peroxidationTME

Identifiers

PMID42163887
PMCPMC13184743

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.