Evidence map›Paper›PMID 42229232›Full record

ArticleRedox biology2026

Attenuated FTO induces necroptosis of alveolar epithelium via the m

Mindan Wu, Wenjing Wang, Zemin Chen, Yuanlan Yang, Jiawei Yan, Yachao Cui, Peiyu Huang, Feng Zhang, Wei Tu, Wensheng Chen and 4 more

Abstract read
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. 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

14 authors.

Mindan WuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Wenjing WangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Zemin ChenState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Yuanlan YangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China; GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Jiawei YanState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China; GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Yachao CuiState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Peiyu HuangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Feng ZhangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Wei TuGuangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Wensheng ChenGuangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China.
Ruiting SunState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China.
Yumin ZhouState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China. Electronic address: zhouyumin410@126.com.
Leqing ZhuGuangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China. Electronic address: zhuleqing1@163.com.
Pixin RanState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, National Center for Respiratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, 510005, China; Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 XingDaoHuanBei Road, Guangzhou, Guangdong, 510005, China. Electronic address: pxran@gzhmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emphysema is a major phenotype of chronic obstructive pulmonary disease (COPD) and reflects sustained oxidative injury and defective alveolar repair in the distal lung. While cigarette smoke is the dominant environmental trigger, endogenous epithelial programs that restrain reactive oxygen species (ROS) and preserve alveolar integrity remain poorly defined in the adult lung parenchyma. Here we identify that fat mass and obesity-associated protein (FTO) as a redox-responsive regulator in the alveolar epithelium. FTO is predominantly expressed in alveolar type II (AT2) epithelial cells and is markedly reduced in both the epithelium of human COPD patients and the lungs of cigarette smoke-exposed mice. This reduction correlated with worse pulmonary function and was inversely associated with cumulative smoking burden in human. Global attenuation of FTO expression resulted in spontaneous emphysema and impaired lung mechanics in mice. Mechanistically, FTO deficiency promotes cytochrome P450 1B1 (CYP1B1) expression via increased m

Indexed as

Alpha-Ketoglutarate-Dependent Dioxygenase FTOAlveolar Epithelial CellsNecroptosisPulmonary EmphysemaAnimalsDisease Models, AnimalHumansMaleMiceOxidative StressPulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesRNA MethylationSignal TransductionAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, humanFTO protein, mouseReactive Oxygen SpeciesAlveolar epitheliumCOPDEmphysemaFTONecroptosisOxidative stress

Identifiers

PMID42229232
PMCPMC13251485

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.