Evidence map›Paper›PMID 41864191›Full record

ArticleRedox biology2026

Copper deprivation reprograms antioxidant defense to suppress ferroptosis via SLC7A11.

Qian Xue, Ziyuan Chen, Jiao Yang, Kaixuan Ren, Xiaofen Li, Xi Chen, Ding Yan, Yuan Wang, Daolin Tang, Jinbao Liu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 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. Article
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

11 authors.

Qian XueGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; State Key Laboratory of Respiratory Disease, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 511436, China.
Ziyuan ChenGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Jiao YangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Kaixuan RenGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Xiaofen LiGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; State Key Laboratory of Respiratory Disease, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 511436, China.
Xi ChenKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; State Key Laboratory of Respiratory Disease, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 511436, China.
Ding YanGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Yuan WangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, 75390, USA.
Jinbao LiuGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; State Key Laboratory of Respiratory Disease, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 511436, China. Electronic address: jliu@gzhmu.edu.cn.
Xin ChenGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China. Electronic address: chenxin@gzhmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copper is an essential trace element that governs diverse cellular functions and influences cell fate. However, how cells adapt to copper deprivation remains poorly understood. Here, we identify a copper-ferroptosis regulatory axis mediated by the cystine transporter SLC7A11. We show that copper loss, induced either by silencing of the copper importer SLC31A1 or by pharmacological chelation, leads to a marked upregulation of SLC7A11. This adaptive response enhances glutathione synthesis, bolsters antioxidant defenses, and protects cells from ferroptosis. Mechanistically, copper deprivation activates AMPK, which stabilizes the transcription factor NRF2 to drive SLC7A11 expression. Functionally, SLC31A1 depletion diminishes ferroptosis-dependent tumor suppression in xenograft models, while dietary copper restriction alleviates ferroptosis-mediated pancreatic injury in experimental acute pancreatitis. Together, these findings reveal copper deprivation as a robust condition driving ferroptosis resistance and suggest that dietary or pharmacological copper modulation could provide new strategies to fine-tune ferroptosis in cancer and tissue injury.

Indexed as

Amino Acid Transport System y+AntioxidantsCation Transport ProteinsCopperFerroptosisAMP-Activated Protein KinasesAnimalsGlutathioneHumansMiceNF-E2-Related Factor 2PancreatitisAmino Acid Transport System y+AMP-Activated Protein KinasesAntioxidantsCation Transport ProteinsCopperGlutathioneNF-E2-Related Factor 2SLC7A11 protein, humanSlc7a11 protein, mouseAMPKCopperFerroptosisNRF2SLC31A1SLC7A11

Identifiers

PMID41864191
PMCPMC13019507

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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.