Evidence map›Paper›PMID 40454481›Full record

ArticleThe Journal of clinical investigation2025

PIEZO1 mediates periostin+ myofibroblast activation and pulmonary fibrosis in mice.

Liran Xu, Ting Li, Yapeng Cao, Yu He, Zehua Shao, Siyu Liu, Bianbian Wang, Ailing Su, Huijing Tian, Yongxin Li and 13 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Multi-omics insights into the mechanisms and prognosis of IPF.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Piezo channels in tumors.Journal of cancer research and clinical oncology · 2026
    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

23 authors.

Liran XuDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Ting LiDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Yapeng CaoDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Yu HeDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Zehua ShaoDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Siyu LiuDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Bianbian WangCenter for Mitochondrial Biology and Medicine, School of Life Science and Technology, and.
Ailing SuBiobank, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Huijing TianDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Yongxin LiDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Guozheng LiangDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Changhe WangCenter for Mitochondrial Biology and Medicine, School of Life Science and Technology, and.
John ShyyDivision of Cardiology, Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Ying XiongDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Fangyuan ChenDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Jason Xj YuanThe Herbert Wertheim UF Scripps Institute, University of Florida, Jupiter, Florida, USA.
Junjun LiuShaanxi Techshake Biotechnology, Xi'an, Shaanxi, China.
Bin ZhouNew Cornerstone Science Laboratory, State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Nina WettschureckDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Stefan OffermannsDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Yang YanDepartment of Cardiac Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education.
Zuyi YuanDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Shengpeng WangDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease characterized by the excessive accumulation of activated myofibroblasts that deposit extracellular matrix (ECM) protein, leading to progressive scar formation and mechanical stress. However, the cellular origin and fate of myofibroblasts remain controversial, and the mechanisms by which myofibroblasts sense mechanical cues in the lung are unclear. Here, we report that periostin (Postn) is a reliable and distinctive marker for pulmonary myofibroblasts, while ablation of Postn+ myofibroblasts after injury ameliorated lung fibrosis. PIEZO1 was highly expressed in Postn+ myofibroblast and played a vital role in mechanoactivation of Postn+ myofibroblast and development of lung fibrosis. Conditional deletion of Piezo1 in Postn+ myofibroblasts significantly inhibited lung fibrosis by suppressing myofibroblast activation and proliferation. Loss of Piezo1 led to disruption of actin organization and prevention of Yap/Taz nuclear localization, thus shifting the myofibroblasts from a proliferative state into a stressed and apoptotic state. Furthermore, myofibroblast-specific Yap/Taz deletion fully recapitulated the protective phenotypes of myofibroblast-Piezo1-KO mice. These findings show that periostin marks pulmonary myofibroblasts, and that PIEZO1-mediated mechanosensation is essential for myofibroblast activation in the lung. Targeting PIEZO1 in the periostin-expressing cells is a novel therapeutic option to interfere with fibrotic diseases such as IPF .

Indexed as

Cell Adhesion MoleculesIdiopathic Pulmonary FibrosisIon ChannelsMechanotransduction, CellularMyofibroblastsPulmonary FibrosisAdaptor Proteins, Signal TransducingAnimalsCell ProliferationLungMiceMice, KnockoutPeriostinYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Adhesion MoleculesIon ChannelsPeriostinPiezo1 protein, mousePostn protein, mouseYap1 protein, mouseYAP-Signaling ProteinsCell biologyFibrosisIon channelsPulmonology

Identifiers

PMID40454481
PMCPMC12126248

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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.