Evidence map›Paper›PMID 35443048›Full record

ArticleBlood2022

Mechanosensation by endothelial PIEZO1 is required for leukocyte diapedesis.

ShengPeng Wang, Bianbian Wang, Yue Shi, Tanja Möller, Rebekka I Stegmeyer, Boris Strilic, Ting Li, Zuyi Yuan, Changhe Wang, Nina Wettschureck and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
12.9field-weighted citation impact, top 1% of its field
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

70 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Mechanisms of Piezo1-Mediated Mechanotransduction in Thrombotic Diseases.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Chemical and Mechanical Regulation of Leukocyte Migration.Cold Spring Harbor perspectives in biology · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

ShengPeng WangDepartment of Cardiology, First Affiliated Hospital, Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.
Bianbian WangCenter for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Yue ShiDepartment of Cardiology, First Affiliated Hospital, Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.
Tanja MöllerDepartment of Vascular Cell Biology, Max Planck Institute of Molecular Biomedicine, Muenster, Germany.
Rebekka I StegmeyerDepartment of Vascular Cell Biology, Max Planck Institute of Molecular Biomedicine, Muenster, Germany.ORCID 0000-0003-0246-5285
Boris StrilicMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Bad Nauheim, Germany.
Ting LiDepartment of Cardiology, First Affiliated Hospital, Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.
Zuyi YuanDepartment of Cardiology, First Affiliated Hospital, Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.
Changhe WangCenter for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Nina WettschureckMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Bad Nauheim, Germany.
Dietmar VestweberDepartment of Vascular Cell Biology, Max Planck Institute of Molecular Biomedicine, Muenster, Germany.ORCID 0000-0002-3517-732X
Stefan OffermannsMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Bad Nauheim, Germany.ORCID 0000-0001-8676-6805
Max Planck Institute for Heart and Lung Research · DEMax Planck Institute for Molecular Biomedicine · DEFirst Affiliated Hospital of Xi'an Jiaotong University · CNGoethe University Frankfurt · DEXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extravasation of leukocytes is a critical step during inflammation that requires the localized opening of the endothelial barrier. This process is initiated by the close interaction of leukocytes with various adhesion molecules such as ICAM-1 on the surface of endothelial cells. Here we reveal that mechanical forces generated by leukocyte-induced clustering of ICAM-1 synergize with fluid shear stress exerted by the flowing blood to increase endothelial plasma membrane tension and to activate the mechanosensitive cation channel PIEZO1. This leads to increases in [Ca2+]i and activation of downstream signaling events including phosphorylation of tyrosine kinases sarcoma (SRC) and protein tyrosine kinase 2 (PYK2), as well as of myosin light chain, resulting in opening of the endothelial barrier. Mice with endothelium-specific Piezo1 deficiency show decreased leukocyte extravasation in different inflammation models. Thus, leukocytes and the hemodynamic microenvironment synergize to mechanically activate endothelial PIEZO1 and subsequent downstream signaling to initiate leukocyte diapedesis.

Indexed as

Ion ChannelsLeukocytesTransendothelial and Transepithelial MigrationAnimalsEndothelial CellsEndothelium, VascularInflammationIntercellular Adhesion Molecule-1MiceIntercellular Adhesion Molecule-1Ion ChannelsPiezo1 protein, mouse

Identifiers

PMID35443048
PMCPMC9305087
OpenAlexW4225585585

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.