Evidence map›Paper›PMID 39487505›Full record

ArticleRespiratory research2024

Loss of interferon regulatory factor-1 prevents lung fibrosis by upregulation of pon1 expression.

Aiyuan Zhou, Xiyan Zhang, Xinyue Hu, Tiao Li, Wenzhong Peng, Hang Yang, Dingding Deng, Chunheng Mo, Rongli Lu, Pinhua Pan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. 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

10 authors.

Aiyuan ZhouDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xiyan ZhangDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xinyue HuDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Tiao LiDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Wenzhong PengDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Hang YangDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Dingding DengDepartment of Respiratory Medicine, First Affiliated People's Hospital of Shaoyang College, Shaoyang, 422001, Hunan, People's Republic of China.
Chunheng MoKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, 610064, China. chunhengmo@gmail.com.
Rongli LuDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. lurongli@csu.edu.cn.
Pinhua PanDepartment of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. pinhuapan668@csu.edu.cn.

Funding

China Postdoctoral Science Foundation 2023M733967National Key Clinical Specialist Construction Program of China z047-02National Natural Science Foundation of China 82300097Natural Science Foundation of Hunan Province 2023JJ41025Project Program of National Clinical Research Center for Geriatric Disorders 2020LNJJ05Scientific Research Project of Hunan Health Commission D202303029041Youth Science Foundation of Xiangya Hospital 2022Q06
6 · The paper itself

Abstract

backgroundInterferon regulatory factor-1 (IRF1) is a transcription factor that plays a significant role in various biological processes, including inflammatory injury, viral infection, cell death, and immune responses, and it has been extensively studied in the context of different lung diseases. However, the mechanism underlying its involvement in lung fibrosis remains largely unknown.

methodsWild type (WT) mice, IRF1 global-null mice (Irf1

resultsIn the bleomycin-induced fibrosis mouse model, increased expression of IRF1 was observed. Irf1 knockout mice displayed decreased lung fibrosis relative to WT mice following treatment with bleomycin. The protein expression of fibronectin, as assessed by the Western blot analysis of lung tissues, was downregulated in Irf1

conclusionOur data highlight the importance of IRF1 in the fibrotic process, and PON1 may be a potential mediator of IRF1 in the progression of lung fibrosis.

Indexed as

AryldialkylphosphataseBleomycinInterferon Regulatory Factor-1Mice, Inbred C57BLMice, KnockoutPulmonary FibrosisUp-RegulationAnimalsFemaleHumansLungMaleMiceAryldialkylphosphataseBleomycinInterferon Regulatory Factor-1IRF1 protein, humanIrf1 protein, mouseFerroptosisIRF1Lung fibrosisPON1

Identifiers

PMID39487505
PMCPMC11529560

What Socratic 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 Socratic graph.