Evidence map›Paper›PMID 41413904›Full record

ArticleJournal of translational medicine2025

Mechanistic study on how the Tet1/ARF-p53 pathway affects idiopathic pulmonary fibrosis through macrophage polarization.

Peng Zhang, Xiaotong Guo, Ting Wang, Shaojin Wang

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Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Peng ZhangDepartment of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, 804 Shengli South Street, Xingqing District, Yinchuan, 750004, China.
Xiaotong GuoDepartment of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, 804 Shengli South Street, Xingqing District, Yinchuan, 750004, China.
Ting WangDepartment of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, 804 Shengli South Street, Xingqing District, Yinchuan, 750004, China.
Shaojin WangDepartment of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, 804 Shengli South Street, Xingqing District, Yinchuan, 750004, China. wangshaojin2025@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aimed to investigate the mechanism by which the Tet1/ARF-p53 pathway affects idiopathic pulmonary fibrosis (IPF) through macrophage polarization.

methodsThe polarization state of macrophages in IPF was analyzed, and the role of the Tet1/ARF-p53 pathway in macrophage polarization was examined. The expression changes of Tet1, ARF, and p53 were detected in both in vitro cell culture and in vivo animal models, as well as the levels of M1 and M2 macrophage markers.

resultsTet1 regulated the DNA methylation status of the ARF gene, thereby affecting ARF expression and subsequently activating the p53 pathway. This regulation affected macrophage polarization, where M2 macrophage polarization was inhibited, ultimately alleviating the progression of pulmonary fibrosis.

conclusionThe Tet1/ARF-p53 pathway plays a role in IPF by regulating macrophage polarization, providing a new potential therapeutic target for IPF.

Indexed as

Cell PolarityCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsIdiopathic Pulmonary FibrosisMacrophagesMixed Function OxygenasesProto-Oncogene ProteinsSignal TransductionTumor Suppressor Protein p53AnimalsDNA MethylationHumansMaleMice, Inbred C57BLCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsMixed Function OxygenasesProto-Oncogene ProteinsTET1 protein, humanTET1 protein, mouseTumor Suppressor Protein p53ARFIdiopathic pulmonary fibrosisMacrophage polarizationp53Tet1

Identifiers

PMID41413904
PMCPMC12903230

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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.