Evidence mapPaperPMID 42426556Full record

ReviewExpert reviews in molecular medicine2026

Convergent Microenvironment Linking Idiopathic Pulmonary Fibrosis and Lung Cancer.

Min Chen, Yeyuan Zhu, Bin Wang, Lijuan Zhang, Boyi Chen, Xuefei Shi, Enhai Cui

Abstract readReview
In one paragraph

Review in Expert reviews in molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Min ChenDepartment of Respiratory Medicine, Affiliated Huzhou Hospital, Zhejiang University School of Medicine, Huzhou, People's Republic of China.
Yeyuan ZhuDepartment of Respiratory Medicine, Huzhou Central Hospital, Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, People's Republic of China.
Bin WangDepartment of Respiratory Medicine, Affiliated Huzhou Hospital, Zhejiang University School of Medicine, Huzhou, People's Republic of China.
Lijuan ZhangDepartment of Respiratory Medicine, Affiliated Huzhou Hospital, Zhejiang University School of Medicine, Huzhou, People's Republic of China.
Boyi ChenDepartment of Respiratory Medicine, Affiliated Huzhou Hospital, Zhejiang University School of Medicine, Huzhou, People's Republic of China.
Xuefei ShiDepartment of Respiratory Medicine, Affiliated Huzhou Hospital, Zhejiang University School of Medicine, Huzhou, People's Republic of China.ORCID https://orcid.org/0000-0002-8065-1887
Enhai CuiDepartment of Respiratory Medicine, Affiliated Huzhou Hospital, Zhejiang University School of Medicine, Huzhou, People's Republic of China.ORCID https://orcid.org/0000-0002-8808-8793

Funding

Basic Public Welfare Research Program of Zhejiang Province Grant NO. WKJ-ZJ-2556Huzhou Municipal Science and Technology Bureau Grant NO. 2022GY02Natural Science Foundation of Zhejiang Province Grant NO. LY22H160038
6 · The paper itself

Abstract

backgroundIdiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease with limited treatment options and a poor prognosis. Lung cancer (LC) is one of the most common comorbidities in IPF, and IPF is recognized as an independent risk factor for the development of LC. In recent years, increasing evidence has suggested that these two diseases may share convergent genetic, epigenetic and cellular mechanisms, particularly within their microenvironments.

methodsA comprehensive literature search was performed across PubMed, Web of Science, and Google Scholar databases to identify relevant studies focusing on the shared cellular components, immune and stromal behaviors, and pathogenic pathways within the microenvironments of IPF and LC.

resultsThis review delineates the convergent features of the IPF and LC microenvironments by synthesizing the functional reprogramming of key cellular constituents. The immunological landscape is characterized by aberrant macrophage polarization, T-cell exhaustion and the accumulation of immunosuppressive myeloid-derived suppressor cells and immature dendritic cells. Furthermore, profound stromal alterations are observed, encompassing fibroblast activation, pathological extracellular matrix remodelling, epithelial-mesenchymal transition and dysregulated angiogenesis. These common cellular and molecular alterations may simultaneously drive fibrosis progression and tumorigenesis.

conclusionsA deeper understanding of the relationship between the IPF and LC microenvironments will help identify shared pathological mechanisms and provide new insights for developing more targeted diagnostic and therapeutic strategies for idiopathic pulmonary fibrosis associated with lung cancer (IPF-LC).

Indexed as

Cellular MicroenvironmentIdiopathic Pulmonary FibrosisLung NeoplasmsTumor MicroenvironmentAnimalsEpithelial-Mesenchymal TransitionHumanscellular plasticityidiopathic pulmonary fibrosislung cancermicroenvironmentpathogenesistherapy

Identifiers

PMID42426556
PMCPMC13472222

What Socratic holds

Textmetadata
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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.