Evidence map›Paper›PMID 40454475›Full record

ArticleThe Journal of clinical investigation2025

PIEZO1 mediates mechanical reprogramming of neutrophils for proangiogenic specialization in the lung.

Jin Wang, Wenying Zhao, Wenjuan Bai, Dong Dong, Hui Wang, Xin Qi, Ajitha Thanabalasuriar, Youqiong Ye, Tian-le Xu, Hecheng Li and 3 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. 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

13 authors.

Jin WangShanghai Institute of Immunology.
Wenying ZhaoShanghai Institute of Immunology.
Wenjuan BaiShanghai Institute of Immunology.
Dong DongDepartment of Thoracic Surgery, Ruijin Hospital, and.
Hui WangShanghai Institute of Immunology.
Xin QiDepartment of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ajitha ThanabalasuriarDepartment of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
Youqiong YeShanghai Institute of Immunology.
Tian-le XuDepartment of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hecheng LiDepartment of Thoracic Surgery, Ruijin Hospital, and.
Paul KubesSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Bin LiShanghai Institute of Immunology.
Jing WangShanghai Institute of Immunology.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are the most abundant immune cells that constantly patrol or marginate inside vascular beds to support immune homeostasis. The extent to which neutrophils undergo reprogramming in response to the changes in vascular architecture and the resultant biological implications of such adaptations remain unclear. Here, we performed intravital imaging and transcriptional profiling to investigate neutrophil behavior across different tissues. Our findings revealed that neutrophils had significant deformability and spontaneous calcium signaling while navigating through the narrow pulmonary vessels. Pulmonary neutrophils exhibited unique transcriptional profiles and were specialized for proangiogenic functions. We found that the mechanosensitive ion channel Piezo-type mechanosensitive ion channel component 1 (PIEZO1) was essential for neutrophil reprogramming. Deletion of Piezo1 in neutrophils ablated the lung-specific proangiogenic transcriptional signature and impaired capillary angiogenesis in both physiological and pathological conditions. Collectively, these data show that mechanical adaptation of neutrophils within the pulmonary vasculature drives their reprogramming in the lungs and promotes pulmonary vascular homeostasis.

Indexed as

Ion ChannelsLungMechanotransduction, CellularNeovascularization, PhysiologicNeutrophilsAnimalsCalcium SignalingHumansMiceMice, KnockoutIon ChannelsPiezo1 protein, mouseImmunologyIon channelsMicrocirculationNeutrophilsPulmonologyVascular biology

Identifiers

PMID40454475
PMCPMC12126238

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.