Evidence map›Paper›PMID 39675497›Full record

ArticleActa biomaterialia2025

PIEZO1-mediated mechanotransduction regulates collagen synthesis on nanostructured 2D and 3D models of fibrosis.

Neda Rashidi, Natalia S Harasymowicz, Alireza Savadipour, Nancy Steward, Ruhang Tang, Sara Oswald, Farshid Guilak

Abstract read
In one paragraph

Article in Acta biomaterialia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
  6. Mechanical compression causes lung hypoplasia in congenital diaphragmatic hernia with GATA4 genetic variants.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. 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

7 authors.

Neda RashidiDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Mechanical Engineering, Washington University, St. Louis, MO 63130, USA.
Natalia S HarasymowiczDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Alireza SavadipourDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Mechanical Engineering, Washington University, St. Louis, MO 63130, USA.
Nancy StewardDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Ruhang TangDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Sara OswaldDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Farshid GuilakDepartment of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Shriners Hospitals for Children, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Mechanical Engineering, Washington University, St. Louis, MO 63130, USA; Cytex Therapeutics, Inc., Durham, NC 27704, USA. Electronic address: guilak@wustl.edu.

Funding

VISCOELASTIC PROPERTIES OF NORMAL AND OA CHONDRONSR01AG015768 · NIA · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 1998 to 2022
$7.7M
Washington University Rheumatic DiseasesResearch Resource-based CenterP30AR073752 · NIAMS · WASHINGTON UNIVERSITY · PI Alfred Hyoungju Kim · 2018 to 2026
$7.6M
Resource Based Center for Musculoskeletal Biology and Medicine (Overall Application)P30AR074992 · NIAMS · WASHINGTON UNIVERSITY · PI MATTHEW J SILVA · 2019 to 2026
$6.8M
Genetically-engineered stem cells for self-regulating arthritis therapyR01AR080902 · NIAMS · WASHINGTON UNIVERSITY · PI Farshid Guilak, Christine T. Pham · 2022 to 2026
$3.7M
OBESITY, BIOMECHANICS, AND INFLAMMATION IN OSTEOARTHRITISR01AG046927 · NIA · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 2013 to 2023
$3.2M
Deconstructing Cartilage Mechanotransduction by Piezo ChannelsR01AR072999 · NIAMS · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 2020 to 2024
$2.9M
TRAINING IN REGENERATIVE MEDICINET32EB028092 · NIBIB · WASHINGTON UNIVERSITY · PI Farshid Guilak · 2020 to 2026
$2.0M
NIAMS NIH HHS P30 AR073752NIAMS NIH HHS P30 AR074992NIAMS NIH HHS R01 AR072999NIAMS NIH HHS R01 AR080902NIA NIH HHS R01 AG015768NIA NIH HHS R01 AG046927NIBIB NIH HHS T32 EB028092
6 · The paper itself

Abstract

Progressive fibrosis can lead to tissue malfunction and organ failure due to the pathologic accumulation of a collagen-rich extracellular matrix. In vitro models provide useful tools for deconstructing the roles of specific biomechanical or biological mechanisms, such as substrate micro- and nanoscale architecture, in these processes for identifying potential therapeutic targets. Here, we investigated how the mechanosensitive ion channel PIEZO1 influences fibrotic gene and protein expression in adipose-derived stem cells (hASCs). Specifically, we examined the role of PIEZO1 and the mechanosensitive transcription factors YAP/TAZ in sensing aligned or non-aligned substrate architecture to regulate collagen formation. We utilized both 2D microphotopatterned substrates and 3D electrospun polycaprolactone (PCL) substrates to study the role of culture dimensionality. We found that PIEZO1 regulates collagen synthesis in hASCs in a manner that is sensitive to substrate architecture. Activation of PIEZO1 induced significant morphological changes in hASCs, particularly when cultured on aligned substrates, leading to a 30-40 % reduction in cell spreading area and increased cell elongation, in 3D-aligned cultures. Picrosirius Red staining and immunoblotting revealed that PIEZO1 activation reduced collagen accumulation in 3D culture. While YAP translocated to the cytoplasm following PIEZO1 activation, depleting YAP and TAZ did not change collagen expression significantly downstream of PIEZO1 activation, implying that YAP/TAZ translocation from the nucleus and decreased collagen synthesis may be independent consequences of PIEZO1 activation. Our studies demonstrate a role for PIEZO1 in cellular mechanosensing of substrate architecture and provide targetable pathways for treating fibrosis and for enhancing tissue-engineered and regenerative approaches for fibrous tissue repair. STATEMENT OF SIGNIFICANCE: This study examines how cells sense and respond to their physical environment via PIEZO1 mechanotransduction. We discovered that cells use PIEZO1 to detect the alignment of surrounding structures, influencing the production of collagen - a key component in fibrosis. Our study used both 2D and 3D models to mimic different tissue environments, providing new insights into how cellular responses change in more complex settings. Importantly, we found that activating PIEZO1 alters cell shape and collagen production, especially on aligned surfaces. Interestingly, while PIEZO1 activation caused YAP translocation to the cytoplasm, this translocation did not directly affect collagen production. This work advances our understanding of fibrosis development and identifies PIEZO1 as a potential target for new therapies.

Indexed as

CollagenIon ChannelsMechanotransduction, CellularModels, BiologicalNanostructuresAdipose TissueFibrosisHumansPolyestersStem CellsTranscription FactorsYAP-Signaling ProteinsCollagenIon ChannelsPIEZO1 protein, humanpolycaprolactonePolyestersTranscription FactorsYAP-Signaling ProteinsCollagenMechanobiologyObesityPIEZO channelsSubstrate architectureYAP/TAZ

Identifiers

PMID39675497
PMCPMC13276715

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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.