Evidence map›Paper›PMID 41663525›Full record

ArticleCellular & molecular immunology2026

GPX4-dependent ferroptosis governs ILC2 homeostasis and colitis progression.

Gaoyu Liu, Ying Wang, Huachen Huang, Jianye Wang, Jinhao Yang, Jingyi Wu, Hailong Cao, Yuxin Zhang, Yuchao Jing, Pan Zhou and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article 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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Gaoyu Liu *Department of Oncology, Laboratory of Immunity, Inflammation & Cancer, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ying Wang *Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Huachen Huang *Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Jianye Wang *Department of Oncology, Laboratory of Immunity, Inflammation & Cancer, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jinhao YangTianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Jingyi WuDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, China.
Hailong CaoDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, China.ORCID 0000-0002-0147-7826
Yuxin ZhangTianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yuchao JingTianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Pan ZhouTianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Ying YuDepartment of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID 0000-0002-6476-1752
Chun ChenDivision of Hematology/Oncology, Department of Pediatrics, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Qiang LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China. qliu@tmu.edu.cn.
Jie ZhouDepartment of Oncology, Laboratory of Immunity, Inflammation & Cancer, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China. zhoujie@tmu.edu.cn.ORCID 0000-0001-5964-1599

Funding

China Postdoctoral Science Foundation No. 2022M713571National Natural Science Foundation of China (National Science Foundation of China) 81925018National Natural Science Foundation of China (National Science Foundation of China) 82130049National Natural Science Foundation of China (National Science Foundation of China) 82171284National Natural Science Foundation of China (National Science Foundation of China) 82201917National Natural Science Foundation of China (National Science Foundation of China) 82225015National Natural Science Foundation of China (National Science Foundation of China) 82321001National Natural Science Foundation of China (National Science Foundation of China) 82430055
6 · The paper itself

Abstract

The critical role of group 2 innate lymphoid cells (ILC2s) in host defense and mucosal inflammation has been well established, yet the mechanisms underlying ILC2 survival and death remain unknown. Here, we report that ILC2s are vulnerable to ferroptosis, as evidenced by an abundance of ferroptosis signature genes and the accumulation of lipid peroxidation in ILC2s. Ablation of glutathione peroxidase 4 (GPX4) in ILC2s (Il5

Indexed as

ColitisDisease ProgressionFerroptosisHomeostasisImmunity, InnateLymphocytesPhospholipid Hydroperoxide Glutathione PeroxidaseAnimalsHumansInflammatory Bowel DiseasesLipid PeroxidationMiceMice, Inbred C57BLMice, KnockoutOxidative Stressglutathione peroxidase 4, mousePhospholipid Hydroperoxide Glutathione PeroxidaseFerroptosisGPX4Group 2 innate lymphoid cellsInflammatory bowel disease

Identifiers

PMID41663525
PMCPMC13036055

What Socratic 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 Socratic graph.