Evidence map›Paper›PMID 41588247›Full record

ReviewCellular & molecular immunology2026

Tackling cuproptosis: from metabolic rewiring to therapeutic exploitation in cancer.

Qian Hao, Yu Gan, Xiang Zhou

Abstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  16. Review
  17. Nanozyme-Driven Ferroptosis-Cuproptosis Interplay in Lung Cancer.International journal of nanomedicine · 2026
    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

3 authors.

Qian Hao *Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Yu Gan *Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Xiang ZhouCancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China. xiangzhou@fudan.edu.cn.ORCID 0000-0002-1172-7948

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82173022National Natural Science Foundation of China (National Science Foundation of China) 82273098National Natural Science Foundation of China (National Science Foundation of China) 82403120National Natural Science Foundation of China (National Science Foundation of China) 82472714
6 · The paper itself

Abstract

Cuproptosis, a recently identified copper-dependent form of regulated cell death, is driven by mitochondrial dysfunction caused by copper overload. Cuproptosis results from proteotoxic stress, which is triggered by copper-induced aggregation of lipoylated tricarboxylic acid (TCA) cycle enzymes and destabilization of iron-sulfur cluster proteins. This review elucidates the mechanisms of cuproptosis, emphasizing its regulation by copper homeostasis, metabolic reprogramming, and key signaling pathways such as p53, HIF-1α, Wnt/β-catenin, and AKT. Notably, copper modulates antitumor immunity through its effects on the tumor microenvironment, suggesting a critical role in cancer immunotherapy. Therapeutic strategies using copper ionophores and nanomedicine platforms demonstrate potential to induce cuproptosis in a variety of cancers. Preclinical studies highlight cuproptosis as a promising strategy against malignancies with copper dysregulation or mitochondrial metabolism adaptation, while clinical translation requires biomarker-driven patient stratification and optimized delivery systems. This synthesis provides a framework for harnessing cuproptosis in precision oncology, bridging mechanistic insights to therapeutic innovation.

Indexed as

CopperCuproptosisNeoplasmsAnimalsHumansMetabolic ReprogrammingMitochondriaProteotoxic StressSignal TransductionTumor MicroenvironmentCopperCancer therapyCuproptosisMetabolismNanomedicineTumor microenvironment

Identifiers

PMID41588247
PMCPMC12949048

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.