Evidence map›Paper›PMID 41326673›Full record

ArticleCommunications biology2025

YOD1 promotes ferroptosis in acute lung injury by deubiquitination of NCOA4.

Xiaopei Yan, Yuqiong Chen, Xinyan Li, Chang Qi, Li Xu, Ying Chen, Chao Huang, Ting Ruan, Guopeng Xu, Chao Chen and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. 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

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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

12 authors.

Xiaopei Yan *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Yuqiong Chen *Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China. cosmoscyq@163.com.ORCID http://orcid.org/0000-0001-7592-5989
Xinyan Li *Center for Precision Cancer Medicine & Translational Research, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Chang Qi *Department of Pathology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Li XuDepartment of Respiratory and Critical Care Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China.
Ying ChenDepartment of Respiratory and Critical Care Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China.
Chao HuangMinistry of Science and Technology / Public Experimental Department, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, China.
Ting RuanDepartment of Respiratory and Critical Care Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China.
Guopeng XuDepartment of Respiratory and Critical Care Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China.
Chao ChenDepartment of Respiratory and Critical Care Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China. chenchao120218@163.com.
Su LiDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China. li.su@zs-hospital.sh.cn.
Xiuqin ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China. zxq92@sina.com.

Funding

China Postdoctoral Science Foundation 2023M731763China Postdoctoral Science Foundation 2024T170427National Natural Science Foundation of China (National Science Foundation of China) 82200449National Natural Science Foundation of China (National Science Foundation of China) 82300479National Natural Science Foundation of China (National Science Foundation of China) 82570495
6 · The paper itself

Abstract

Acute lung injury (ALI) is a prevalent critical condition for which effective treatments remain elusive. Ferroptosis plays a significant role in the pathophysiology of ALI. The deubiquitinating enzyme YOD1 is implicated in the regulation of infectious diseases; however, its specific role in ALI and ferroptosis is not yet fully understood. In this study, we observed that YOD1 expression was notably elevated in the lung tissue and primary alveolar type II (ATII) cells of mice subjected to lipopolysaccharide (LPS)-induced ALI. Moreover, YOD1 deficiency significantly mitigated ferroptosis and damage to the alveolar epithelial barrier. Mechanistically, YOD1 interacts directly with NCOA4 through its OTU domain, inhibiting K48-linked ubiquitination at the K343/K353 lysis residue of NCOA4, thus facilitating NCOA4-mediated autophagic degradation of FTH1 and promoting ferroptosis. Overall, our findings indicate that YOD1 regulates NCOA4 via deubiquitination, suggesting it may serve as a potential therapeutic target for ALI.

Indexed as

Acute Lung InjuryFerroptosisNuclear Receptor CoactivatorsAnimalsAutophagyHumansLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutUbiquitinationLipopolysaccharidesNuclear Receptor Coactivators

Identifiers

PMID41326673
PMCPMC12769745

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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.