Evidence map›Paper›PMID 39928535›Full record

ArticleJournal of cellular and molecular medicine2025

Single Cell RNA-Seq Identifies Cell Subpopulations Contributing to Idiopathic Pulmonary Fibrosis in Humans.

Tangjuan Zhang, Zhichao Hou, Zheng Ding, Peng Wang, Xue Pan, Xiangnan Li

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Multi-omics reveals a novel Cxcr4Clinical and translational medicine · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Immunosenescence in Idiopathic Pulmonary Fibrosis.Journal of inflammation research · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  12. Article
  13. Review
  14. 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

6 authors.

Tangjuan ZhangDepartment of Emergency, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zhichao HouDepartment of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zheng DingDepartment of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Peng WangSchool of Nursing and Health, Zhengzhou University, Zhengzhou, China.
Xue PanSchool of Nursing and Health, Zhengzhou University, Zhengzhou, China.
Xiangnan LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0009-0006-2855-5528

Funding

Engineering Laboratory 2021-1013Henan Province Medical Science and Technology Research Plan Joint Construction Projects LHGJ20190027Henan Province Medical Science and Technology Research Plan Joint Construction Projects LHGJ20190109Henan Province Medical Science and Technology Research Plan Joint Construction Projects SBGJ202002110National Natural Science Foundation of China 32070623Provinces and Ministry of Education Joint Construction SBGJ202002015Zhengzhou University's Advanced Medical Research Center
6 · The paper itself

Abstract

The cell populations, particularly subpopulations, involved in the onset and progression of idiopathic pulmonary fibrosis (IPF) remain incompletely understood. This study employed single-cell RNA-seq to identify cell populations and subpopulations with significantly altered proportions in the lungs of patients with IPF. In IPF lungs, endothelial cell proportions were significantly increased, while alveolar epithelial cell proportions were markedly decreased. Among the three identified fibroblast subpopulations, the proportion of myofibroblasts was significantly increased, while the proportions of the other two fibroblast subtypes were reduced. Similarly, within the three macrophage subpopulations, the macrophage_SPP1 subpopulation, localised to fibroblastic foci, showed a significant increase in proportion, while the alveolar macrophage subpopulation was significantly reduced. Trajectory analysis revealed that fibroblasts in IPF lungs could differentiate into myofibroblasts, and alveolar macrophages could transition into the macrophage_SPP1 subpopulation. Among T-cell subpopulations, only the CD4 T_FOXP3 subpopulation exhibited a significant change, whereas all four B-cell subpopulations showed significant proportional shifts. These findings provide a comprehensive view of the cellular alterations contributing to IPF pathogenesis. Extensive interactions among various cell populations and subpopulations were identified. The proportions of various cell populations and subpopulations in IPF lungs, including endothelial cells, fibroblasts, macrophages and B cells, were significantly altered. Further in-depth investigation into the roles of cell subpopulations with significantly altered proportions in the onset and progression of IPF will provide valuable insights into the pathological mechanisms underlying the disease. This understanding could facilitate the development of novel therapeutic strategies and medications for IPF treatment.

Indexed as

Idiopathic Pulmonary FibrosisRNA-SeqSingle-Cell AnalysisAgedBiomarkersB-LymphocytesEndothelial CellsFemaleFibroblastsHumansLungMacrophagesMacrophages, AlveolarMaleMiddle AgedMyofibroblastsBiomarkerscell–cell interactionend‐stage lung diseasefibroblastidiopathic pulmonary fibrosisinterstitial lung diseasemacrophagescRNA‐seqT and B cells

Identifiers

PMID39928535
PMCPMC11809556

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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 OpenQuestion graph.